x curso de ́n mecánica en anestesia, cuidados intensivos y ... · x curso de ventilación...
TRANSCRIPT
X Curso de Ventilacio n Mecanica en Anestesia, Cuidados Intensivos y Trasplantes
Antonio Romero Berrocal
Fisiología-Fisiopatología: Vasorreactividad y autorregulación.
Hiperventilación- Hiperoxia.
VM en paciente neuroquirúrgico. Craneotomía con sedación.
PEEP y efectos sobre la PIC.
Extubación y traqueotomía.
TCE: - Manejo ventilatorio. VPP.
- TCE y trauma pulmonar: SDRA neurogénico.
- TCE y trauma abdominal: Sd. Compartimental.
ACTUALIZACIÓN EN VENTILACIO N MECA NICA EN NEUROCIRUGÍA.
Fisiología-Fisiopatología: Vasorreactividad y autorregulación.
Hiperventilación- Hiperoxia.
VM en paciente neuroquirúrgico. Craneotomía con sedación.
PEEP y efectos sobre la PIC.
Extubación y traqueotomía.
TCE: - Manejo ventilatorio. VPP.
- TCE y trauma pulmonar: SDRA neurogénico.
- TCE y trauma abdominal: Sd. Compartimental.
ACTUALIZACIÓN EN VENTILACIO N MECA NICA EN NEUROCIRUGÍA.
FSC.
PPC= PAM-PIC.
20% consumo total de O2.
Elastancia / Complianza.
CO2: - hipercapnia-vasodilatación: FSC, PIC.
- hipocapnia-vasoconstricción: FSC, PIC.
pH del LCR.
Autorregulación: 50-150 mmHg. Ajuste requiere hasta 3min.
Mantenida con LOE.
Isquemia, Hipoxia, TCE , Anestésicos.
VASORREACTIVIDAD.
Prospectivo. N=186. TCE grave
Hiperventilación: PIC, PAM, SjvO2, Pbto2 y FSC.
Hiperoxia: Sjvo2 y Pbto2.
PIC leve ,pCO2 y EtCO2.
12 pacientes sanos. Inhalación aire-CO2 4%/ Hiperventilación.
Vasoconstricción reactiva a hipocapnia, no tanto a hipercapnia.
No hay diferencias en la vasorreactividad al CO2 para pCO2
30-40 mmHg.
Menor reactividad en niñas para pCO2 50 mmHg.
Parece que la vasculatura de las niñas es más sensible a la vasodilatación del sevorane para MAC<1.
ORIGIN A L A RTICLE
Gender di f f erences in cerebrovascular react iv i t y t o carbon
diox ide dur ing sevofl urane anest hesia in chi ldren:
prel im inary fi ndings
Arunotai Siriussawakul1, Deepak Sharma2, Pimwan Sookplung1, William Armstead3 &
Monica S. Vavilala4
1 Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA, USA
2 Departments of Anesthesiology and Pain Medicine and Neurological Surgery, University of Washington, Seattle, WA, USA
3 Departments of Anesthesiology and Critical Care, University of Pennsylvania, Philadelphia, PA, USA
4 Departments of Anesthesiology and Pain Medicine, Pediatrics, Neurological Surgery and Radiology, University of Washington, Seattle,
WA, USA
Introduct ion
Cerebrovascular reactivity to carbon dioxide (CO2R) is
the intrinsic property of cerebral vasculature to respond
to changes in arterial carbon dioxide tension and leads
to changes in cerebral blood flow and cerebral blood
volume. The effect of hyperventilation, which is fre-
quently utilized by the anesthesiologists to provide in-
traoperative brain relaxation in patients with reduced
intracranial compliance, may be affected by CO2R.
While CO2R may be impaired by a variety of patho-
logical conditions and its absence may indicate a poor
outcome (1), it can also be affected by age, gender and
anesthetic agents even in healthy individuals. CO2R is
Keyw ords
cerebrovascular carbon dioxide reactivity;
children; gender
Correspondence
Monica S. Vavilala,
Associate Professor of Anesthesiology &
Pediatrics, Harborview Medical Center, 325
Ninth Avenue, Box 359724, Seattle, WA
98104, USA
Email: [email protected]
Section Editor: Jerrold Lerman
Accepted 24 November 2010
doi:10.1111/j.1460-9592.2010.03498.x
Summary
Background: Cerebrovascular reactivity to carbon dioxide (CO2R) is
affected by age, gender and anesthetic agents. While gender differences in
CO2R are described in adults, there are no such data in children.
Aim: To examine the gender differences in CO2R in children during sevo-
flurane anesthesia.
Methods: Five girls and five boys < 15 years of age and ASA physical sta-
tus I , undergoing general anesthesia for elective surgery were enrolled.
Under steady-state anesthesia with < 1.0 M AC sevoflurane, middle cerebral
artery blood flow velocity changes were monitored using Transcranial
Doppler ultrasound while endtidal carbon dioxide (EtCO2) was adjusted
from 40 to 30 mmHg (hypocapnia) and then from 40 to 50 mmHg (hyper-
capnia). CO2R was calculated between EtCO2 ranges 30–40 and 40–
50 mmHg. Cerebrovascular resistance (eCVR) was estimated as M AP/
Vmca and the change in eCVR (DeCVR) between EtCO2 30 and 40 mmHg
and between EtCO2 40 and 50 mmHg was calculated.
Results: There was no gender difference in CO2R. However, both CO2R
and DeCVR were lower in the EtCO2 40–50 mmHg range compared to
EtCO2 30–40 mmHg range only in girls (P = 0.01 and P = 0.01, respec-
tively). Vmca increased significantly with increase in CO2 (P < 0.001) for
both boys and girls. The coefficient of nonlinear correlation (r) between
Vmca and EtCO2 was 0.88 in girls vs 0.66 in boys.
Conclusion: While there were no gender differences in CO2R within the
individual EtCO2 ranges examined, girls but not boys had a significantly
lower CO2R and DeCVR in the higher EtCO2 range during < 1.0 M AC
sevoflurane anesthesia.
Pediatric Anesthesia ISSN 1155-5645
Pediatric Anesthesia 21 (2011) 141–147 ª 2011 Blackwell Publishing Ltd 141
RMN cuantifica FSC y Resist. Cerebrovascular. Relación lineal
Hipercapnia-FSC y pCO2.
El isoflurano (1,5 MAC) tiene efectos sobre TAM y la autorregulación del FSC en hipertensos.
Autorregulación no variable con la edad.
Conclusión: la evaluación de la autorregulación cerebral y la
PPC óptima es factible en pacientes con HSA y puede
proporcionar información importante a largo plazo.
Una PPC por debajo del rango o una autorregulación
deteriorada se asocia a peor pronostico.
La monitorización intraoperatoria de la autorregulación
cerebral es una consideración importante para pacientes con enfermedades neurológicas.
El Doppler Transcraneal estático parece ser el método de cabecera mejor para este propósito.
Conclusión: La de la cabeza produce:
- significativo de la PIC y la PPC en pacientes con hemorragia cerebral.
- SrO2 dependiendo del grado de elevación de la cabeza.
Conclusiones: Cabecero a 30º: - PIC y mejora de la PPC (no significativa). - Ausencia de cualquier efecto adverso en la dinámica de la PIC, así como en la oxigenación cerebral global y local en pacientes con infarto agudo o TCE, hasta 24 horas después de la lesión.
12 posiciones distintas, 4 tienen cambios en la PIC.
DL: PIC.
Supino: PIC.
Sólo DLI PPC significativamente.
Fisiología-Fisiopatología: Vasorreactividad y autorregulación.
Hiperventilación- Hiperoxia.
VM en paciente neuroquirúrgico. Craneotomía con sedación.
PEEP y efectos sobre la PIC.
Extubación y traqueotomía.
TCE: - Manejo ventilatorio. VPP.
- TCE y trauma pulmonar: SDRA neurogénico.
- TCE y trauma abdominal: Sd. Compartimental.
ACTUALIZACIÓN EN VENTILACIO N MECA NICA EN NEUROCIRUGÍA.
Conclusión: no hay ninguna prueba de que la hipocapnia
mejore los resultados neurológicos en cualquier contexto .
Evidencia III Monitorizar PIC, PbtO2, SjvO2 Mediadores de isquemia tras 30 min. de hiperventilación.
Períodos cortos de hipocapnia moderada ayudan a conseguir
una PPC óptima.
Hiperventilación moderada ,sólo si es sostenida, disminuye la
PIC y la distensibilidad arterial cerebral, agravando la isquemia también.
La hiperventilación moderada mejora el campo quirúrgico y la PIC
durante la craneotomía para la extirpación de tumores supratentoriales.
Conclusión: EtCO2 subestima en ciertos momentos el valor de
la PaCO2 durante la craneotomía, aunque hay correlación
pCO2-EtCO2 en gran parte de la cirugía.
Buena correlación pCO2-EtCO2 en caídas de PAM<20%.
Si PAM baja >30% el gradiente aumenta.
En TCE, la hiperoxia incrementa PbO2 con un efecto variable
sobre el lactato y la relación lactato/piruvato (sobre el metabolismo).
Recientes mediciones directas de CMRO2 en pacientes con TCE
indican que no hay beneficio.
Este hallazgo, junto con su potencial toxicidad debe IMPEDIR
su uso clínico rutinario.
Fisiología-Fisiopatología: Vasorreactividad y autorregulación.
Hiperventilación- Hiperoxia.
VM en paciente neuroquirúrgico. Craneotomía con sedación.
PEEP y efectos sobre la PIC.
Extubación y traqueotomía.
TCE: - Manejo ventilatorio. VPP.
- TCE y trauma pulmonar: SDRA neurogénico.
- TCE y trauma abdominal: Sd. Compartimental.
ACTUALIZACIÓN EN VENTILACIO N MECA NICA EN NEUROCIRUGÍA.
Lesión córtex-médula post: hipoV-apnea: controlada.
Tronco-puente-mesencéfalo: hiperV/hipoV: control-asistida.
Médula: 55%. Cervical C5C6: controlada.
Parada respiratoria 1 semana después de la recuperación.
Special Cases: M echanical Ventilation
of Neurosurgical Patients
Victoria E. Johnson, M Da, Jason H. Huang, M Db,* ,Webster H. Pilcher, M D, PhDb
aThe University of Pennsylvania, Department of Neurosurgery, 105 Hayden Hall,
3320 Smith Walk, Philadelphia, PA 19104, USAbDepartment of Neurosurgery, University of Rochester, 601 Elmwood Avenue,
Box 670 Rochester, NY 14642, USA
M echanical ventilat ion first was developed at the turn of the 20th cen-
tury. I t was not until the 1950s, however, that it became an important
part of clinical practice, a necessity driven by the poliomyeli tis epidemic
in Europe [1]. Since then, mechanical ventilation as a technology has ad-
vanced greatly and is now employed across several specialties, with applica-
tions tailored to the needs of different disease states. A large multinat ional
study demonstrated that approximately 20% of all patients who require me-
chanical ventilat ion do so as a result of neurological dysfunction [2]. Neuro-
critical care is a comparatively new subspecialty that hasemerged to manage
the specific needs of this patient subpopulation, of which appropriate me-
chanical ventilat ion is an important aspect. Neurosurgical patients, particu-
larly victims of traumatic brain injury (TBI), comprise a significant portion
of admissions to such units and require unique consideration. The types of
ventilation and indications for their use, as well as appropriate monitoring,
are imperative to the successful management of these patients. Various
aspects of the strategies of mechanical ventilation applied to neurosurgical
patients remain controversial.
Summary of relevant physiology and pathophysiology
In understanding the aims and indications for endotracheal intubation
and mechanical ventilation, it is necessary to comprehend the underlying
* Corresponding author.
E-mail address: [email protected] (J.H. Huang).
0749-0704/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.ccc.2006.12.003 criticalcare.theclinics.com
Crit Care Clin 23 (2007) 275–290
Special Cases: Mechanical Ventilation
of Neurosurgical Patients
Victoria E. Johnson, MDa, Jason H. Huang, MDb,*,Webster H. Pilcher, MD, PhDb
aThe University of Pennsylvania, Department of Neurosurgery, 105 Hayden Hall,
3320 Smith Walk, Philadelphia, PA 19104, USAbDepartment of Neurosurgery, University of Rochester, 601 Elmwood Avenue,
Box 670 Rochester, NY 14642, USA
Mechanical ventilation first was developed at the turn of the 20th cen-
tury. I t was not until the 1950s, however, that it became an important
part of clinical practice, a necessity driven by the poliomyelitis epidemic
in Europe [1]. Since then, mechanical ventilation as a technology has ad-
vanced greatly and is now employed across several specialties, with applica-
tions tailored to the needs of different disease states. A large multinational
study demonstrated that approximately 20% of all patientswho requireme-
chanical ventilation do so asa result of neurological dysfunction [2]. Neuro-
critical care isa comparatively new subspecialty that hasemerged to manage
the specific needs of this patient subpopulation, of which appropriate me-
chanical ventilation is an important aspect. Neurosurgical patients, particu-
larly victims of traumatic brain injury (TBI), comprise a significant portion
of admissions to such units and require unique consideration. The types of
ventilation and indications for their use, as well as appropriate monitoring,
are imperative to the successful management of these patients. Various
aspects of the strategies of mechanical ventilation applied to neurosurgical
patients remain controversial.
Summary of relevant physiology and pathophysiology
In understanding the aims and indications for endotracheal intubation
and mechanical ventilation, it is necessary to comprehend the underlying
* Corresponding author.
E-mail address: [email protected] (J.H. Huang).
0749-0704/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.ccc.2006.12.003 criticalcare.theclinics.com
Crit Care Clin 23 (2007) 275–290
pCO2 anormal después de un TCE severo se correlaciona con
un mortalidad hospitalaria.
Con TCE o lesiones cerebrales se puede realizar VPP .
Control hipercapnia
En pacientes con HTIC la seguridad de la VPP no está bien
establecida.
Monitorización.
En la serie de 11 pac. el reclutamiento y aumento de la PEEP fue
un método seguro para mejorar la oxigenación.
Siempre se debe monitorizar la PIC.
Fisiología-Fisiopatología: Vasorreactividad y autorregulación.
Hiperventilación- Hiperoxia.
VM en paciente neuroquirúrgico. Craneotomía con sedación.
PEEP y efectos sobre la PIC.
Extubación y traqueostomía.
TCE: - Manejo ventilatorio. VPP.
- TCE y trauma pulmonar: SDRA neurogénico.
- TCE y trauma abdominal: Sd. Compartimental.
ACTUALIZACIÓN EN VENTILACIO N MECA NICA EN NEUROCIRUGÍA.
La respuesta de la PIC y la PPC a la MRA es variable.
En lesión cerebral grave los pacientes con ALI / SDRA,
requieren monitorización continua de la MAP, PIC y PPC
durante el cambio de PEEP o MRA para mejorar la seguridad.
Original Contribution
Impact of positive end-expiratory pressure on cerebral
injury patients with hypoxemia
Xiang-yu Zhang MD⁎, Zi-j ian Yang MD, Qi-xing Wang RRT, Hai-rong Fan MD
Department of Emergency and Critical Care Medicine, Shanghai Tenth People's Hospital,
Tongji University School of Medicine, Shanghai 200072, P.R. China
Received 16 January 2010; revised 27 January 2010; accepted 28 January 2010
Abstract
Background: Traumatic brain injury or intracranial hemorrhage patients with acute lung injury/acute
respiratory distress syndrome need mechanical ventilation. The use of positive end-expiratory pressure
(PEEP) in this situation remains controversial. This study explored the impact of PEEP on intracranial
pressure (ICP), cerebral perfusion pressure (CPP), central venous pressure (CVP), and mean arterial
pressure (MAP) in cerebral injury patients.
Methods: Nine cerebral injury patients with lung injury who needed mechanical ventilation and met the
criteria for ICP monitoring were included in this study. Intraventricular catheters were positioned in 1 of
the bilateral ventricles and connected to pressure transducers. Invasive arterial pressure and CVP were
monitored continuously. Pressure control ventilation was applied during this clinical trial in a stepwise
recruitment maneuver (RM) with 3 cm H2O intermittent increments and decrements of PEEP.
Results: A total of 28 RMs were completed in 9 patients. Mean values of MAP, CVP, ICP, and CPP 5
minutes after RMs showed no significant differences compared with baseline (P N 0.05). Correlation
analysis of all the mean values of MAP, CVP, ICP, and CPP showed significant correlation between
MAP and CPP, PEEP and CVP, PEEP and ICP, and PEEP and CPP with all P values less than 0.05.
Conclusion: The impact of PEEP on blood pressure, ICP, and CPP varies greatly in cerebral injury
patients. Mean arterial pressure and ICP monitoring is of benefit when using PEEP in cerebral injury
patients with hypoxemia.
© 2011 Elsevier Inc. All rights reserved.
Traumatic brain injury or intracranial hemorrhagepatients
with acute lung injury/acute respiratory distress syndrome
(ALI/ARDS) need mechanical ventilation support. This
presents a dilemma for clinical caregivers. To maintain
oxygenation, it is occasionally necessary to perform lung
recruitment maneuvers (RMs) [1,2], to recruit collapsed
pulmonary alveoli using a high airway pressure followed by
appropriate positive end-expiratory pressure (PEEP) to
maintain the recruited alveoli open. However, high intratho-
racic pressure impedes venous blood return to right atrium
and decreases the preload, resulting in diminished cardiac
output [3]. In addition, dueto theimpedanceof venousblood
flow, intracranial pressure (ICP) may be elevated and be
detrimental to brain injury patients. Although alargenumber
of experimental and clinical studies have been conducted,
there is still controversy [4,5] regarding the management of
intracranial hypertension and cerebral edema when a high
airway pressure is used especially with lung RM for ARDS.
How to treat these patients appropriately and balance the
benefits and risks is acontinuing issue in clinical care. From⁎Corresponding author. Tel.: +86 21 66307174; fax: +86 21 66301051.
E-mail address: [email protected] (X. Zhang).
www.elsevier.com/locate/ajem
0735-6757/$ – see front matter © 2011 Elsevier Inc. All rights reserved.
doi:10.1016/j.ajem.2010.01.042
American Journal of Emergency Medicine (2011) 29, 699–703
Original Contribution
Impact of positive end-expiratory pressure on cerebral
injury patients with hypoxemia
Xiang-yu Zhang MD⁎, Zi-jian Yang MD, Qi-xing Wang RRT, Hai-rong Fan MD
Department of Emergency and Critical Care Medicine, Shanghai Tenth People's Hospital,
Tongji University School of Medicine, Shanghai 200072, P.R. China
Received 16 January 2010; revised 27 January 2010; accepted 28 January 2010
Abstract
Background: Traumatic brain injury or intracranial hemorrhage patients with acute lung injury/acute
respiratory distress syndrome need mechanical ventilation. The use of positive end-expiratory pressure
(PEEP) in this situation remains controversial. This study explored the impact of PEEP on intracranial
pressure (ICP), cerebral perfusion pressure (CPP), central venous pressure (CVP), and mean arterial
pressure (MAP) in cerebral injury patients.
Methods: Ninecerebral injury patientswith lung injury who needed mechanical ventilation and met the
criteria for ICPmonitoring wereincluded in thisstudy. Intraventricular catheterswerepositioned in 1 of
the bilateral ventricles and connected to pressure transducers. Invasive arterial pressure and CVP were
monitored continuously. Pressure control ventilation was applied during this clinical trial in a stepwise
recruitment maneuver (RM) with 3 cm H2O intermittent increments and decrements of PEEP.
Results: A total of 28 RMswerecompleted in 9 patients. Mean values of MAP, CVP, ICP, and CPP5
minutes after RMs showed no significant differences compared with baseline (P N 0.05). Correlation
analysis of all the mean values of MAP, CVP, ICP, and CPP showed significant correlation between
MAP and CPP, PEEP and CVP, PEEP and ICP, and PEEP and CPP with all P values less than 0.05.
Conclusion: The impact of PEEP on blood pressure, ICP, and CPP varies greatly in cerebral injury
patients. Mean arterial pressure and ICP monitoring is of benefit when using PEEP in cerebral injury
patients with hypoxemia.
© 2011 Elsevier Inc. All rights reserved.
Traumaticbrain injury or intracranial hemorrhagepatients
with acute lung injury/acute respiratory distress syndrome
(ALI/ARDS) need mechanical ventilation support. This
presents a dilemma for clinical caregivers. To maintain
oxygenation, it is occasionally necessary to perform lung
recruitment maneuvers (RMs) [1,2], to recruit collapsed
pulmonary alveoli using ahigh airway pressure followed by
appropriate positive end-expiratory pressure (PEEP) to
maintain therecruited alveoli open. However, high intratho-
racic pressure impedes venous blood return to right atrium
and decreases the preload, resulting in diminished cardiac
output [3]. Inaddition, dueto theimpedanceof venousblood
flow, intracranial pressure (ICP) may be elevated and be
detrimental tobrain injury patients. Although alargenumber
of experimental and clinical studies have been conducted,
there is still controversy [4,5] regarding the management of
intracranial hypertension and cerebral edema when a high
airway pressure isused especially with lung RM for ARDS.
How to treat these patients appropriately and balance the
benefitsand risks isacontinuing issuein clinical care. From⁎Corresponding author. Tel.: +862166307174; fax: +862166301051.
E-mail address: [email protected] (X. Zhang).
www.elsevier.com/locate/ajem
0735-6757/$ – see front matter © 2011 Elsevier Inc. All rights reserved.
doi:10.1016/j.ajem.2010.01.042
American Journal of Emergency Medicine (2011) 29, 699–703
En TCE, la estrategia de aumentar la PEEP para mejorar la oxigenación no se asocia a reducción de la PPC o del transporte de O2.
accordingly. These changes were significant. Similarly,
PAOP increased with elevating levels of PEEP.
PEEP versus CI, DO2i, and VO2iUnlike the patterns exerted by PEEP on CVP and PAOP,
systemic oxygen kinetics remained unaffected (Table 1). As
PEEP increased, CI remained the same. There were no iden-
tifiable differences in hemoglobin levels among patients (data
not shown). When DO2i and VO2i were examined, these
systemic parameters showed no changes in response to rising
PEEP.
DISCUSSIONOur results showed that in trauma patients with severe
head injury, the strategy of increasing PEEP to optimize
oxygenation was not associated with a reduction in oxygen
transport or worsening of intracranial hypertension. We ob-
served that as PEEP levels increased, CVP and PAOP mea-
surements were accordingly elevated, whereas CI, DO2i, and
VO2i remained unaffected. In relation to brain-specific pres-
sures, increases in PEEP correlated with reduction in ICP,
and augmented CPP. These data support judicious use of
PEEP to maximize oxygen transport in the management of
head-injured patients with concomitant acute lung injury.
Application of PEEP in the care of critically ill patients
after TBI remains controversial. Clinically, PEEP exerts ben-
eficial effects on oxygenation by increasing functional resid-
ual capacity, reducing intrapulmonary shunt via alveolar re-
cruitment, and lowering supplemental oxygen.7 Excessive
PEEP can create volutrauma, hamper venous drainage, re-
duce MAP, and increase ICP.9,12,13 These deleterious effects
can worsen CPP, and can negatively impact a head-injured
patient. Presently, the influence of PEEP on brain-specific
pressures, hemodynamics, and oxygen transport after TBI
remains to be established.
In patients with acute respiratory distress syndrome, the
effect of PEEP on hemodynamic parameters has been well
documented.14,15 Elevated airway and pleural pressure result-
ing from increases in PEEP may cause artificially inflated
CVP and PAOP.16 This may lead to a false sense of assurance
that the intravascular status is “adequate.” Our data support
previous observations showing increases in CVP and PAOP
corresponding to elevating levels of PEEP. Furthermore, we
found that oxygen transport in our study remained unaffected,
despite changes in PEEP levels.
Optimized oxygen transport parameters (e.g., CI, DO2i,
and VO2i) have resulted in survival benefits.17–20 However,
other clinical trials of a heterogeneous group of patients with
unclear timing of resuscitation have demonstrated no
difference21 or higher mortality rates using high doses of
inotropic support.22 In addition, these calculated values have
been shown to be less affected by PEEP,23 compared with
CVP or PAOP values. Incorporated in our goal-directed re-
suscitation regimen, we found that despite increases in PEEP
levels, oxygen transport parameters (CI, DO2i, and VO2i)
remained unchanged in our head-injured patients. This is
attributable to the endpoints selected on our trauma services
being CI, DO2i, and VO2i, as opposed to CVP or PAOP.
Thus far, our findings agree with previously published
data regarding the effects of PEEP on hemodynamic indices
(CVP and PAOP) and oxygen transport endpoints. Evidence
Table 1 PEEP vs. Cranial Pressures and Oxygen Kinetics (Mean SE)
PEEP (cm H2O) ICP (mm Hg) CPP (mm Hg) CI (L/min/m2) DO2i (mL O2/min/m2) DO2i (mL O2/min/m2)
0–5 14.7 0.2 77.5 0.3* 3.8 0.1 593 9 167 6
6–10 13.6 0.2 80.1 0.5 4.0 0.1 629 21 167 6
11–15 13.1 0.3‡ 78.9 0.7‡ 3.8 0.1 560 21 153 6
* p 0.001 vs. PEEP 6–10 cm H2O; ‡ p 0.001 vs. PEEP 0–5 cm H2O.
Fig. 1. Effects of PEEP on CVP and PAOP. Data are mean SE.
(PEEP 0–5 cmH2O: CVP, 5.9 0.1 mmHg; PEEP 6–10 cmH2O:
CVP, 8.3 0.2 mmHg; PEEP 11–15 cmH2O: CVP, 12.0 0.3 mm
Hg). * p 0.001 compared with PEEP 0 to 5 cm H2O; †p 0.001
vs. PEEP 6 to 10 cm H2O; * * p 0.001 vs. PEEP 0 to 5 cm H2O;
‡p 0.001 compared with PEEP 6 to 10 cm H2O. As PEEP levels
were elevated, both CVP and PAOP increased.
TheJournal of TRAUMA Injury, Infection, andCritical Care
490 September 2002
En HSA PEEP>20 cmH2O puede PAM y PPC.
PEEP no afecta per se a la PIC pero sí indirectamente al PAM y PPC.
En HSA grave valorar retirar la PEEP ante HTIC. Con HD estable la PEEP no afecta a PPC. Necesario monitorización HD.
Con PIC normal: PEEP
- 5cm H2O: no afecta a PIC.
- 10-15cm H2O: PPC no se afecta (>60mmHg). Dudoso efecto en PIC.
Con HITC la PEEP no afecta a PPC ni PIC.
Respuesta HD variable.
PEEP inefectiva para prevenir embolismo gaseoso.
El uso de PEEP no se recomienda para la prevención de la
embolia gaseosa.
Fisiología-Fisiopatología: Vasorreactividad y autorregulación.
Hiperventilación- Hiperoxia.
VM en paciente neuroquirúrgico. Craneotomía con sedación.
PEEP y efectos sobre la PIC.
Extubación y traqueotomía.
TCE: - Manejo ventilatorio. VPP.
- TCE y trauma pulmonar: SDRA neurogénico.
- TCE y trauma abdominal: Sd. Compartimental.
ACTUALIZACIÓN EN VENTILACIO N MECA NICA EN NEUROCIRUGÍA.
La traqueostomi a precoz (≤9 dias) en neurocri ticos aporta
ventajas: dias de VM y estancia en UCI y menores
requerimientos de sedacio n y de antibioterapia.
La traqueostomía tardi a no se relaciona directamente con la
mortalidad, pero riesgo de padecer neumonia.
Neurocirugía
214
2010;;
2
1
: Neurocirugía
215
2010;;
2
1
:
Análisis d
e
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ueot omía prec
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im
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a
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ncia
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o
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.
. 211-22 1
Tabla 2
Comparación entre TRQ precoz y TRQ tardía en relación con el tiempo de intubación orotraqueal hasta la realiza-
ción d
e
TRQ
TRQ ≤
9
día
s
TRQ>9 dí as p
(
n=
5
3
)
(n
=
6
5)
E
d
a
d
52.1±19.6 52.5±19.0 0.901
Se
x
o
( nº,
%
) : Masculino 31(58.5%) 47(72.3%) 0.115
Femenino 22(41.5%) 18(27.7%)
Di
a
g
nós t i co ( nº,
%
) : TCE
26(49.1%) 45(69.2%) 0.026
ACVA 27(50.9%) 20(30.8%)
Apache I
I
19.2±5.6 19.1±6.0 0.899
GC
S 7.1 ±3. 2 7 .4 ±3. 6 0.784
IO
T h
a
sta la TRQ (d ) 7.1±1.5 15.6±7.7
<
0
.
0
0
1
Ventilación m
e
cáni ca (d
)
14.1±8.5 25.2±15.1
<
0
.0 0 1
VM po s t TRQ (d ) 6 .9 ±9. 2 9 .5 ±12. 9 0.243
Se
d
a
ci ón ( d)
8.1±5.3 17.2±12.2 < 0 .
0
0
1
Antimicrobianos (
d
) 15.4±11.6 25.4±14.6
<0
.
0
0
1
Pa
c
i
entes con
NA V (
n
º ,%) 27(50.9%) 54(83.1%)
< 0 .
0
0
1
Es
t
a
nci a en
U
CI
(
d ) 20.7±10.2 31.2±16.3 < 0 .0 0 1
Es
t
a
nci a hosp
i
t al ari a (d) 48.6±30.6 49.62±27.9 0.844
Mo
r
t
alidad UCI
( nº,%
)
6(11.3%) 7 (1 0. 8%) 0.924
Mo
r
t
alidad hosp
i
t al ari a (nº,%
)
11(20.8%) 12(18.5%) 0.754
TCE: traumatismo craneoencefálico. ACVA: accidente cerebrovascular agudo. VM: ventilación mecánica. IOT: intubación orotraqueal. TRQ: Traqueotomía. NAV: neumonía asociada a ventilación mecánica. GCS: Glasgow coma score. Cuando corresponde los valores se expresan c
omo me
d
i a ±
d
esv
i
aci ón es tán
d
ar de la
med
i
a.
(
d) : día
s
.
Tabla 3
Comparación e
n
t r e pa ci ent es con TCE y ACVA
TCE ACVA p
(
n
=
71) (n=47)
E
d
a
d
47.3±21.4 59.9±12.2
<
0
.
0
0
1
Se
x
o
masc
u
l ino ( nº,%
)
49 (6 9%) 29 (6 1. 7%) 0.411
Apache I
I
18.9±5.3 19.4±6.5 0.676
IO
T h
a
sta la TRQ (d ) 12.2±6.9 11.8±10.3 0.835
Ventilación m
e
cáni ca (d
)
21.4±12.1 18.5±16.2 0.287
VM po s t TRQ (d ) 9 .2 ±1 1.1 8 .2 ±15. 4 0.691
TRQ≤ 9
dí
a
s (nº
,
%) 26 (3 6. 6%) 27 (5 7. 4%) 0.026
Se
d
a
ci ón ( día
s
) 15.7±11.4 9 .2 ±8. 3 0.001
Antimicrobianos (
d
) 24.4±14.4 15.9±13.1 0.002
Pa
c
i
entes con
NA V (
n
º ,%) 53 (7 4. 6%) 28 (5 9. 6%) 0.084
Es
t
a
nci a en
U
CI
(
d ) 28.6±13.6 23.3±16.2 0.059
Es
t
a
nci a hosp
i
t al ari a (d) 47.1±24.2 52.2±34.5 0.347
Mo
r
t
alidad UCI
( nº,%
)
6
(8.5 %)
7
(14. 9%) 0.274
Mo
rt
alidad hosp
i
t al ari a (nº,%
)
10 (1 4. 1%) 13 (2 7. 7%) 0.068
TCE: traumatismo craneoencefálico. ACVA: accidente cerebrovascular agudo. VM: ventilación mecánica. IOT: intubación orotraqueal. TRQ: traqueotomía. NAV: neumonía asociada a ventilación mecánica. Cuando corresponde los valores se expresan como media ± desvia-ción e
stándar de
la
medi
a
. (d):
días.
Neurocirugía
2
2010;;
2
1
:
Recibido:
211
Neurocirugía
2010;;
2
1
:
Resumen
Objetivos. Analizar el momento más adecuado para
la realización de la traqueotomía en enfermos neuro-
críticos, comparando en una población seleccionada
de pacientes las diferencias de morbimortalidad y
consumo de recursos entre el grupo en que se realizó la
traqueotomía precozmente (≤9 días) y aquéllos en los
que f
u
e má
s
tar
d
í a ( >9
dí as)
.
Material y métodos. Estudio prospectivo y observa-
cional en una población de pacientes con diagnóstico
de traumatismo craneoencefálico (TCE) o accidente
cerebrovascular (ACVA) que precisaron traqueotomía
durante su ingreso en UCI . Se compararon los datos
en dos grupos de pacientes: a) traqueotomía precoz
(TP) en los primeros 9 días;;
b) traqueotomía tardía
(TT) a partir del 10º día. Variables estudiadas: datos
demográ fic
o
s, gravedad al ingreso, procedencia, diag-
nóstico, duración de la intubación orotraqueal (IOT)
y de la ventilación mecánica (VM), necesidades de
sedación y de antibioterapia, frecuencia de neumonía
asociada a ventilación mecánica (NAV), duración de la
estancia y mortalidad. Se calculó el riesgo relativo de
padecer neumonía y un modelo de regresión logística
multivariante para determinar los factores asociados
al desarrollo de neumonía. Signi fica ción estadística
para u
n
a p≤
0
. 05.
Resultados. Se estudiaron 118 pacientes, 60% con
TCE. La media de IOT previa a la traqueotomía (TRQ)
fue de 12 días y la duración de la VM de 20 días. Se
diagnosticaron 94 episodios de NAV en 81 pacientes
(68.6%). El grupo de TP muestra menor duración de la
VM, de la sedación, de la antibioterapia y de la estancia
en UCI, con menor incidencia de neumonía (p<0.001).
La precocidad de la TRQ no in fluy ó en la duración de la
estancia hospitalaria (p=0.844), ni en la mortalidad en
UCI (p=0.924), ni en la hospitalaria (p=0.754). La media
de edad fue menor en el grupo con TCE (p<0.001),
además la TRQ se realiza más tarde (p=0.026) y requie-
ren más días de sedación (p=0.001) y de tratamiento
antibiótico (p=0.002). Los factores independientemente
asociados con el desarrollo de neumonía fueron los días
de IOT (p=0.034, OR 1.177) y los días de estancia en
UCI (p=0.003, OR 1.100). El riesgo relativo de pade-
cer neumonía si la TRQ se realiza después de 9 días es
1.55 mayor (IC 95%: 1.10-2
.
16) . Número necesario de
pacientes a tratar (NNT) para que la TRQ precoz evite
un episodio de neumonía: 3.13. La presencia de NAV no
se asocia con una mayor mortalidad en UCI (p=0.558)
ni h
o
spi tal ari a (p
=
0. 370) .
Conclusiones. La traqueotomía precoz (≤9 días) en
los enfermos neurocríticos aporta ventajas apreciables,
acortando los días de ventilación mecánica y de estancia
en UCI, con menores requerimientos de sedación y de
antibioterapia. Aunque la TRQ más tardía no se rela-
ciona directamente con la mortalidad, se eleva conside-
rablemente el riesgo de padecer neumonía, de manera
especial en pacientes con TCE. Estas circunstancias
clínicas deben valorarse individualmente en cada caso a
fin
de establecer el momento más adecuado para practi-
car la TRQ en lo
s
pac
i
entes neur ocríticos.
PALABRAS CLAVE: Traqueotomía. Traqueotomía
precoz. Neurocríticos. Neumonía asociada a ventilación
mecánica.
Analysis of early tracheostomy and its impact on deve-
lopment of pneumonia, use of resources and mortality
in n
e
ur ocritically i
l
l pa
t
i ents
Análisis de la traqueotomía precoz y su impacto sobre la incidencia de neumonía,
consumo d
e
r ecursos y
mor t ali dad en
paci
e
ntes neur ocríticos
Abreviaturas. ACVA: accidente cerebrovascular agudo. APACHE
II: acute physiology and chronic health evaluation. EPOC:
enfermedad pulmonar obstructiva crónica. GCS: Glasgow coma
score. IOT: intubación orotraqueal. NAV: neumonía asociada
a ventilación mecánica. NNT: número necesario de pacientes
a tratar. PIC: presión intracraneal. RR: riesgo relativo. TCE:
traumantismo craneoencefálico. TP: traqueotomía precoz. TRQ:
traqueotomía. TT: traqueotomía tardía. UCI: unidad de cuidados
intensivos. V
M
: ve
n
t i laci ón mec
á
ni ca.
F. G
a
ndí a- Ma
r
t ínez; ; I
.
M
artí
n
ez-Gi l ;;
D. Andaluz-Oj eda; ; F . Bo bi llo de Lamo ; ; L. Pa rra- Morais y F . Dí ez- Gut i érrez
211-2
2
1
Servicio d
e
Me
d
i cina Int
e
nsi va. Hosp
i
t al Clíni
c
o Uni ver
s
i tar io de Valladolid.
3
1
- 07
-
09 . Aceptado;; 1 9- 01-
10
Neurocirugía
2
2010;;
2
1
:
Recibido:
211
Neurocirugía
2010;;
2
1
:
Resumen
Objetivos. Analizar el momento más adecuado para
la realización de la traqueotomía en enfermos neuro-
críticos, comparando en una población seleccionada
de pacientes las diferencias de morbimortalidad y
consumo de recursos entre el grupo en que se realizó la
traqueotomía precozmente (≤9 días) y aquéllos en los
que f
u
e má
s
tar
d
í a ( >9
dí as)
.
Material y métodos. Estudio prospectivo y observa-
cional en una población de pacientes con diagnóstico
de traumatismo craneoencefálico (TCE) o accidente
cerebrovascular (ACVA) que precisaron traqueotomía
durante su ingreso en UCI. Se compararon los datos
en dos grupos de pacientes: a) traqueotomía precoz
(TP) en los primeros 9 días;;
b) traqueotomía tardía
(TT) a partir del 10º día. Variables estudiadas: datos
demográ fic
o
s, gravedad al ingreso, procedencia, diag-
nóstico, duración de la intubación orotraqueal (IOT)
y de la ventilación mecánica (VM), necesidades de
sedación y de antibioterapia, frecuencia de neumonía
asociada a ventilación mecánica (NAV), duración de la
estancia y mortalidad. Se calculó el riesgo relativo de
padecer neumonía y un modelo de regresión logística
multivariante para determinar los factores asociados
al desarrollo de neumonía. Signi fica ción estadística
para u
n
a p≤
0
. 05.
Resultados. Se estudiaron 118 pacientes, 60% con
TCE. La media de IOT previa a la traqueotomía (TRQ)
fue de 12 días y la duración de la VM de 20 días. Se
diagnosticaron 94 episodios de NAV en 81 pacientes
(68.6%). El grupo de TP muestra menor duración de la
VM, de la sedación, de la antibioterapia y de la estancia
en UCI, con menor incidencia de neumonía (p<0.001).
La precocidad de la TRQ no influy ó en la duración de la
estancia hospitalaria (p=0.844), ni en la mortalidad en
UCI (p=0.924), ni en la hospitalaria (p=0.754). La media
de edad fue menor en el grupo con TCE (p<0.001),
además la TRQ se realiza más tarde (p=0.026) y requie-
ren más días de sedación (p=0.001) y de tratamiento
antibiótico (p=0.002). Los factores independientemente
asociados con el desarrollo de neumonía fueron los días
de IOT (p=0.034, OR 1.177) y los días de estancia en
UCI (p=0.003, OR 1.100). El riesgo relativo de pade-
cer neumonía si la TRQ se realiza después de 9 días es
1.55 mayor (IC 95%: 1.10-2
.
16) . Número necesario de
pacientes a tratar (NNT) para que la TRQ precoz evite
un episodio de neumonía: 3.13. La presencia de NAV no
se asocia con una mayor mortalidad en UCI (p=0.558)
ni h
o
spi tal ari a (p
=
0. 370) .
Conclusiones. La traqueotomía precoz (≤9 días) en
los enfermos neurocríticos aporta ventajas apreciables,
acortando los días de ventilación mecánica y de estancia
en UCI, con menores requerimientos de sedación y de
antibioterapia. Aunque la TRQ más tardía no se rela-
ciona directamente con la mortalidad, se eleva conside-
rablemente el riesgo de padecer neumonía, de manera
especial en pacientes con TCE. Estas circunstancias
clínicas deben valorarse individualmente en cada caso a
fin
de establecer el momento más adecuado para practi-
car la TRQ en lo
s
pac
i
entes neur ocríticos.
PALABRAS CLAVE: Traqueotomía. Traqueotomía
precoz. Neurocríticos. Neumonía asociada a ventilación
mecánica.
Analysis of early tracheostomy and its impact on deve-
lopment of pneumonia, use of resources and mortality
in n
e
ur ocritically i
l
l pa
t
i ents
Análisis de la traqueotomía precoz y su impacto sobre la incidencia de neumonía,
consumo d
e
r ecursos y
mor t ali dad en
paci
e
ntes neur ocríticos
Abreviaturas. ACVA: accidente cerebrovascular agudo. APACHE
II: acute physiology and chronic health evaluation. EPOC:
enfermedad pulmonar obstructiva crónica. GCS: Glasgow coma
score. IOT: intubación orotraqueal. NAV: neumonía asociada
a ventilación mecánica. NNT: número necesario de pacientes
a tratar. PIC: presión intracraneal. RR: riesgo relativo. TCE:
traumantismo craneoencefálico. TP: traqueotomía precoz. TRQ:
traqueotomía. TT: traqueotomía tardía. UCI: unidad de cuidados
intensivos. V
M
: ve
n
t i laci ón mec
á
ni ca.
F. G
a
ndí a-Ma
r
t ínez; ; I
.
M
artí
n
ez-Gi l ;;
D. Andaluz-Oj eda; ; F . Bo bi llo de Lamo ; ; L. Pa rra- Morais y F . Dí ez-Gut i érrez
211-2
2
1
Servicio d
e
Me
d
i cina Int
e
nsi va. Hosp
i
t al Clíni
c
o Uni ver
s
i tar io de Valladolid.
3
1
- 07
-
09 . Aceptado;; 1 9- 01-
10
Neurocirugía
2
2010;;
2
1
:
Recibido:
211
Neurocirugía
2010;;
2
1
:
Resumen
Objetivos. Analizar el momento más adecuado para
la realización de la traqueotomía en enfermos neuro-
críticos, comparando en una población seleccionada
de pacientes las diferencias de morbimortalidad y
consumo de recursos entre el grupo en que se realizó la
traqueotomía precozmente (≤9 días) y aquéllos en los
que f
u
e má
s
tar
d
í a ( >9
dí as)
.
Material y métodos. Estudio prospectivo y observa-
cional en una población de pacientes con diagnóstico
de traumatismo craneoencefálico (TCE) o accidente
cerebrovascular (ACVA) que precisaron traqueotomía
durante su ingreso en UCI. Se compararon los datos
en dos grupos de pacientes: a) traqueotomía precoz
(TP) en los primeros 9 días;;
b) traqueotomía tardía
(TT) a partir del 10º día. Variables estudiadas: datos
demográ fic
o
s, gravedad al ingreso, procedencia, diag-
nóstico, duración de la intubación orotraqueal (IOT)
y de la ventilación mecánica (VM), necesidades de
sedación y de antibioterapia, frecuencia de neumonía
asociada a ventilación mecánica (NAV), duración de la
estancia y mortalidad. Se calculó el riesgo relativo de
padecer neumonía y un modelo de regresión logística
multivariante para determinar los factores asociados
al desarrollo de neumonía. Signi fica ción estadística
para u
n
a p≤
0
. 05.
Resultados. Se estudiaron 118 pacientes, 60% con
TCE. La media de IOT previa a la traqueotomía (TRQ)
fue de 12 días y la duración de la VM de 20 días. Se
diagnosticaron 94 episodios de NAV en 81 pacientes
(68.6%). El grupo de TP muestra menor duración de la
VM, de la sedación, de la antibioterapia y de la estancia
en UCI, con menor incidencia de neumonía (p<0.001).
La precocidad de la TRQ no in fluy ó en la duración de la
estancia hospitalaria (p=0.844), ni en la mortalidad en
UCI (p=0.924), ni en la hospitalaria (p=0.754). La media
de edad fue menor en el grupo con TCE (p<0.001),
además la TRQ se realiza más tarde (p=0.026) y requie-
ren más días de sedación (p=0.001) y de tratamiento
antibiótico (p=0.002). Los factores independientemente
asociados con el desarrollo de neumonía fueron los días
de IOT (p=0.034, OR 1.177) y los días de estancia en
UCI (p=0.003, OR 1.100). El riesgo relativo de pade-
cer neumonía si la TRQ se realiza después de 9 días es
1.55 mayor (IC 95%: 1.10-2
.
16) . Número necesario de
pacientes a tratar (NNT) para que la TRQ precoz evite
un episodio de neumonía: 3.13. La presencia de NAV no
se asocia con una mayor mortalidad en UCI (p=0.558)
ni h
o
spi tal ar i a (p
=
0. 370) .
Conclusiones. La traqueotomía precoz (≤9 días) en
los enfermos neurocríticos aporta ventajas apreciables,
acortando los días de ventilación mecánica y de estancia
en UCI, con menores requerimientos de sedación y de
antibioterapia. Aunque la TRQ más tardía no se rela-
ciona directamente con la mortalidad, se eleva conside-
rablemente el riesgo de padecer neumonía, de manera
especial en pacientes con TCE. Estas circunstancias
clínicas deben valorarse individualmente en cada caso a
fin
de establecer el momento más adecuado para practi-
car la TRQ en lo
s
pac
i
entes neur ocríticos.
PALABRAS CLAVE: Traqueotomía. Traqueotomía
precoz. Neurocríticos. Neumonía asociada a ventilación
mecánica.
Analysis of early tracheostomy and its impact on deve-
lopment of pneumonia, use of resources and mortality
in n
e
ur ocritically i
l
l pa
t
i ents
Análisis de la traqueotomía precoz y su impacto sobre la incidencia de neumonía,
consumo d
e
r ecursos y
mor t ali dad en
paci
e
ntes neur ocríticos
Abreviaturas. ACVA: accidente cerebrovascular agudo. APACHE
II: acute physiology and chronic health evaluation. EPOC:
enfermedad pulmonar obstructiva crónica. GCS: Glasgow coma
score. IOT: intubación orotraqueal. NAV: neumonía asociada
a ventilación mecánica. NNT: número necesario de pacientes
a tratar. PIC: presión intracraneal. RR: riesgo relativo. TCE:
traumantismo craneoencefálico. TP: traqueotomía precoz. TRQ:
traqueotomía. TT: traqueotomía tardía. UCI: unidad de cuidados
intensivos. V
M
: ve
n
t i laci ón mec
á
ni ca.
F. G
a
ndí a- Ma
r
t ínez; ; I
.
M
artí
n
ez-Gi l ;;
D. Andaluz-Oj eda; ; F . Bo bi llo de Lamo ; ; L. Pa rra- Morais y F . Dí ez- Gut i érrez
211-2
2
1
Servicio d
e
Me
d
i cina Int
e
nsi va. Hosp
i
t al Clíni
c
o Uni ver
s
i tar io de Valladolid.
3
1
- 07
-
09 . Aceptado;; 1 9- 01-
10
En TCE, traqueostomía precoz estancia en UCI, hospitalización, neumonía y duración del uso de antibióticos.
La protocolización sistemática del destete y extubación tasa
de reintubación por fallo en extubación, sin afectar a la
duración de la VM y es bien aceptado por el personal de UCI.
Revisión del destete en UCI quirúrgica.
Escala de Glasgow no relacionada al fracaso de la extubación.
Reflejos respiratorios (tos), obedecer ordenes, secreciones.
Traqueostomia: evidencia para demorarla en caso de HTIC o mala PPC.
Traqueostomia temprana.
Liberation of neurosurgical patients from mechanical
venti lation and tracheostomy in neurocrit ical care,
Christos Lazaridis MDa,⁎, Stacia M. DeSantis PhDb, Marc McLawhorn MSc,Vibhor Krishna MDd
aDepartment of Neurosciences-Neurosciences Critical Care, Medical University of South Carolina, Charleston,
SC 29425, USAbDepartment of Biostatistics, Medical University of South Carolina, Charleston, SC 29425, USAcMedical University of South Carolina, Charleston, SC 29425, USAdDepartment of Neurosurgery, Medical University of South Carolina, Charleston, SC 29425, USA
Keywords:Mechanical ventilation;
Brain injury;
Ventilator liberation;
Extubation
Abstract Neurosurgical patients commonly require mechanical ventilation and monitoring in a
neurocritical careunit. There areonly few studies that specifically address the process of liberation from
mechanical ventilation in this population. Patients who remain ventilator or artificial airway dependent
receive a tracheostomy. The appropriate timing for the procedure is not well defined and may be
different among an inhomogeneous population of critically ill patients. In this article, we review the
general principles of liberation and the current literature as it pertains to neurosurgical patients with
primary brain injury. The criteria for “ readiness of extubation” include a combination of neurologic
assessment, hemodynamic, and respiratory parameters. Future studies are required to better assess
indicators for extubation readiness, evaluate thepredictors of extubation failure in brain-injured patients,
and define the most appropriate timing for a tracheostomy.
© 2011 Elsevier Inc. All rights reserved.
1. Introduction
Neurosurgical patients commonly require mechanical
ventilation (MV) and monitoring in a neurocritical care
unit (NCCU). The purpose of MV is to maintain ventilation,
optimize oxygenation, and protect the airway. Most patients
can be liberated from MV as soon as they recover from the
acute physiologic derangement or postoperative state that
brought them to the intensive care unit (ICU). Nevertheless,
5% to 20% of all ICU patients remain ventilator dependent
for at least 7 days [1]. Prolonged MV is associated with
significant complications that increase morbidity and
mortality and generate significant financial and logistic
burdens. Some common complications include ventilator-
associated pneumonia, ventilator-induced lung injury, air-
way injury, ventilator-induced diaphragmatic dysfunction,
and prolonged immobility. Here, we will discuss the
principles of liberation from MV and review the current
clinical literature, as it pertains to patientswith primary brain
injury in the NCCU.
Financial disclosures: None. Funding disclosure: None.⁎Corresponding author. Division of Neurosciences Critical Care,
Departments of Neurology and Neurosurgery, Medical University of
South Carolina, Charleston, SC 29425, USA. Tel.: +1 843 792 3221; fax:
+1 843 876 8626.
E-mail address: [email protected] (C. Lazaridis).
0883-9441/$ – see front matter © 2011 Elsevier Inc. All rights reserved.
doi:10.1016/j.jcrc.2011.08.018
Journal of Critical Care (2011) xx, xxx–xxx
Liberation of neurosurgical patients from mechanical
ventilation and tracheostomy in neurocritical care,
Christos Lazaridis MDa,⁎, Stacia M. DeSantis PhDb, Marc McLawhorn MSc,Vibhor Krishna MDd
aDepartment of Neurosciences-Neurosciences Critical Care, Medical University of South Carolina, Charleston,
SC 29425, USAbDepartment of Biostatistics, Medical University of South Carolina, Charleston, SC 29425, USAcMedical University of South Carolina, Charleston, SC 29425, USAdDepartment of Neurosurgery, Medical University of South Carolina, Charleston, SC 29425, USA
Keywords:Mechanical ventilation;
Brain injury;
Ventilator liberation;
Extubation
Abstract Neurosurgical patients commonly require mechanical ventilation and monitoring in a
neurocritical careunit. Thereareonly few studies that specifically address theprocessof liberation from
mechanical ventilation in this population. Patients who remain ventilator or artificial airway dependent
receive a tracheostomy. The appropriate timing for the procedure is not well defined and may be
different among an inhomogeneous population of critically ill patients. In this article, we review the
general principles of liberation and the current literature as it pertains to neurosurgical patients with
primary brain injury. The criteria for “readiness of extubation” include a combination of neurologic
assessment, hemodynamic, and respiratory parameters. Future studies are required to better assess
indicators for extubation readiness, evaluate thepredictorsof extubation failure in brain-injured patients,
and define the most appropriate timing for a tracheostomy.
© 2011 Elsevier Inc. All rights reserved.
1. Introduction
Neurosurgical patients commonly require mechanical
ventilation (MV) and monitoring in a neurocritical care
unit (NCCU). Thepurposeof MV is to maintain ventilation,
optimize oxygenation, and protect theairway. Most patients
can be liberated from MV as soon as they recover from the
acute physiologic derangement or postoperative state that
brought them to the intensive careunit (ICU). Nevertheless,
5% to 20% of all ICU patients remain ventilator dependent
for at least 7 days [1]. Prolonged MV is associated with
significant complications that increase morbidity and
mortality and generate significant financial and logistic
burdens. Some common complications include ventilator-
associated pneumonia, ventilator-induced lung injury, air-
way injury, ventilator-induced diaphragmatic dysfunction,
and prolonged immobility. Here, we will discuss the
principles of liberation from MV and review the current
clinical literature, asit pertainsto patientswith primary brain
injury in the NCCU.
Financial disclosures: None. Funding disclosure: None.⁎Corresponding author. Division of Neurosciences Critical Care,
Departments of Neurology and Neurosurgery, Medical University of
South Carolina, Charleston, SC 29425, USA. Tel.: +1 843 792 3221; fax:
+1 843 876 8626.
E-mail address: [email protected] (C. Lazaridis).
0883-9441/$ – see front matter © 2011 Elsevier Inc. All rights reserved.
doi:10.1016/j.jcrc.2011.08.018
Journal of Critical Care (2011) xx, xxx–xxx
ISSN 0100-879X
BI O M EDI CAL SCI ENCESAND
CL I NI CAL I NVEST I GAT I ONwww.bjournal.com .brwww.bjournal.com .br
Volum e 44 (12) 1194-1298 Decem ber 2011
Institutional Sponsors
The Brazilian Journal of Medical and Biological Research is partially financed by
All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License
Faculdade de Medicina de Ribeirão Preto
CampusRibeirão Preto
Explore High - Perform ance MS
Orbit rap Technology
I n Proteom ics & Metabolom ics
analiticaweb.com.br S C I E N T I F I C
Braz J M ed Biol Res, Decem ber 2011, Volum e 44(12) 1291-1298
doi: 10.1590/S0100-879X2011007500146
Implications of extubation failure and prolonged mechanical ventilation in the postoperative period following elective intracranial surgery
M.C. Vidotto, L.C. Sogame, M.R. Gazzotti, M. Prandini and J.R. Jardim
ISSN 0100-879X
BI OM EDI CAL SCI ENCESAND
CL INI CAL INVEST I GAT I ONwww.bjournal.com.brwww.bjournal.com.br
Volume 44 (12) 1194-1298 Decem ber 2011
Institutional Sponsors
The Brazilian Journal of Medical and Biological Research is partially financed by
All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License
Faculdade de Medicina de Ribeirão Preto
CampusRibeirão Preto
Explore High - Perform ance MS
Orbitrap Technology
I n Proteom ics & Metabolom ics
analiticaweb.com.br S C I E N T I F I C
Braz J M ed Biol Res, December 2011, Volume 44(12) 1291-1298
doi: 10.1590/S0100-879X2011007500146
Implications of extubation failure and prolonged mechanical ventilation in the postoperative period following elective intracranial surgery
M.C. Vidotto, L.C. Sogame, M.R. Gazzotti, M. Prandini and J.R. Jardim
El retraso en la extubación en cirugía programada no mejora los
parametros HD ni metabólicos.
In Group I: extubated as soon as possible in the recovery room
after surgery.
In Group II: sedated with propofol for 2 h
PjVO2 y la PA de la A. Cerebral media junto a PAM, con
mantenimiento de la entrega de oxígeno cerebral.
Los cambios en flujos y presiones cerebrales se asocian con
preservación de la oxigenación cerebral.
El transitorio en PIC y PAM no afecta a la oxigenación cerebral.
Fisiología-Fisiopatología: Vasorreactividad y autorregulación.
Hiperventilación- Hiperoxia.
VM en paciente neuroquirúrgico. Craneotomía con sedación.
PEEP y efectos sobre la PIC.
Extubación y traqueotomía.
TCE: - Manejo ventilatorio. VPP.
- TCE y trauma pulmonar: SDRA neurogénico.
- TCE y trauma abdominal: Sd. Compartimental.
ACTUALIZACIÓN EN VENTILACIO N MECA NICA EN NEUROCIRUGÍA.
ALI factor de riesgo independiente para SEPSIS.
estancia en UCI y costes.
PbtO2 buena guía para comprobar la mejora en la oxigenación
cerebral en TCE.
Un tratamiento que mejore la PbtO2 puede relacionarse con
mejor supervivencia.
La aplicación de PbtO2-CCG en este centro de neurotrauma, significativamente la mortalidad y mejora el manejo en TCE a los 6 meses.
La severidad del TCE, dificultad en el control de la PIC y la mala PPC >48 h son los factores predictores de mortalidad más importantes.
Parece que con PIC >50 , >36h. Puede ser efectivo el manejo
agresivo de la PIC y PPC.
No hiperventilar.
Peep óptima con monitorización HD y PIC.
Seguridad de VPP: evitar hipercapnia.
Intensive Care Med (2006) 32:1925–1927DOI 10.1007/s00134-006-0407-z EDITORIAL
Luciana Mascia Ventilatory setting in severe brain injuredpatients: does it really matter?
Received: 18 September 2006Accepted: 18 September 2006Published online: 20 October 2006© Springer-Verlag 2006
This editorial refers to the article available at:http://dx.doi.org/10.1007/s00134-006-0406-0
This work was supported by EEC grants QLCT-2000-00454and QLCT-2002-001160
L. Mascia ()Università di Torino, Dipartimento di Anestesiologia eRianimazione,Ospedale S. Giovanni Battista, Corso Dogliotti 14, 10126 Turin,Italye-mail: [email protected].: +39-011-6335600Fax: +39-011-6960448
Introduction
The presence of pulmonary dysfunction in severe braininjury is a well known phenomenon. Development ofacute lung injury/acute respiratory distress syndrome(ALI/ARDS) occurs in 20–25% of patients with isolatedbrain injury, both subarachnoid hemorrhage and trauma,and is associated with a threefold increased risk of dyingand increased ICU length of stay [1, 2, 3]. Intensive CareMedicine now present an elegant physiological studycarried out by Koutsoukou and coworkers [4] to assessrespiratory mechanics in the early phase after severebrain injury. The authors conclude that on the first dayof mechanical ventilation patients with brain damageexhibit abnormal respiratory mechanics. Static elastanceand minimal resistance further increased after 5 days inpatients ventilated on zero end-expiratory pressure (ZEEP)
while it remained stable in patients ventilated with a mod-erate level of positive end expiratory pressure (PEEP). Inthe present editorial we discuss: (a) the mechanisms ofpulmonary dysfunction, (b) its clinical relevance, and (c)the potential “conflict of interest” between the protectiveventilation strategy for ALI/ARDS and the ventilatorysettings proposed for brain injured patients.
Mechanisms of pulmonary dysfunction
The risk of developing ALI/ARDS after severe brain in-jury was identified by poorer global initial computed to-mography findings [1] and lower Glasgow Coma Scale [5,6] (intracranial factors) together with the administration ofvasoactive drugs and history of drug abuse (extracranialfactors) [2]. Several mechanisms have been postulated ascauses of pulmonary dysfunction, including aspiration, in-fection, and neurogenic pulmonary edema. In the past theoccurrence of neurogenic pulmonary edema has been at-tributed to a hydrostatic phenomenon induced by a mas-sive increase in sympathetic activity [7, 8, 9]; active pul-monary venocostriction together with an altered capillarypermeability may contribute to an increase in extravascularlung water. Rogers and coworkers [8] confirmed in a largeautopsy database a significant increase in the weight of thelungs but not of other organs in patients dying immediatelyor within 96 h from isolated brain injury. Recently it hasbeen suggested that after acute brain injury there is both anincreased intracranial production of proinflammatory cy-tokines resulting in a secondary injury to the brain [10] andthe release of proinflammatory mediators into the systemiccirculation [11]. Yildirim and coworkers [12] reported thatultrastructural damage occurred in type II pneumocyte ina model of traumatic brain injury, suggesting that an acutesystemic inflammatory response plays an integral role inthe development of such injury by initiating infiltration of
Intensive Care Med (2006) 32:1925–1927DOI 10.1007/s00134-006-0407-z EDITORIAL
Luciana Mascia Ventilatory setting in severe brain injuredpatients: does it really matter?
Received: 18 September 2006Accepted: 18 September 2006Published online: 20 October 2006© Springer-Verlag 2006
This editorial refers to the article available at:http://dx.doi.org/10.1007/s00134-006-0406-0
This work was supported by EEC grants QLCT-2000-00454and QLCT-2002-001160
L. Mascia ()Università di Torino, Dipartimento di Anestesiologia eRianimazione,Ospedale S. Giovanni Battista, Corso Dogliotti 14, 10126 Turin,Italye-mail: [email protected].: +39-011-6335600Fax: +39-011-6960448
Introduction
The presence of pulmonary dysfunction in severe braininjury is a well known phenomenon. Development ofacute lung injury/acute respiratory distress syndrome(ALI/ARDS) occurs in 20–25% of patients with isolatedbrain injury, both subarachnoid hemorrhage and trauma,and is associated with a threefold increased risk of dyingand increased ICU length of stay [1, 2, 3]. IntensiveCareMedicine now present an elegant physiological studycarried out by Koutsoukou and coworkers [4] to assessrespiratory mechanics in the early phase after severebrain injury. The authors conclude that on the first dayof mechanical ventilation patients with brain damageexhibit abnormal respiratory mechanics. Static elastanceand minimal resistance further increased after 5 days inpatients ventilated on zero end-expiratory pressure (ZEEP)
while it remained stable in patients ventilated with a mod-erate level of positive end expiratory pressure (PEEP). Inthe present editorial we discuss: (a) the mechanisms ofpulmonary dysfunction, (b) its clinical relevance, and (c)the potential “conflict of interest” between the protectiveventilation strategy for ALI/ARDS and the ventilatorysettings proposed for brain injured patients.
Mechanisms of pulmonarydysfunction
The risk of developing ALI/ARDS after severe brain in-jury was identified by poorer global initial computed to-mography findings [1] and lower Glasgow Coma Scale [5,6] (intracranial factors) together with the administration ofvasoactive drugs and history of drug abuse (extracranialfactors) [2]. Several mechanisms have been postulated ascauses of pulmonary dysfunction, including aspiration, in-fection, and neurogenic pulmonary edema. In the past theoccurrence of neurogenic pulmonary edema has been at-tributed to a hydrostatic phenomenon induced by a mas-sive increase in sympathetic activity [7, 8, 9]; active pul-monary venocostriction together with an altered capillarypermeability may contribute to an increase in extravascularlung water. Rogers and coworkers [8] confirmed in a largeautopsy database a significant increase in the weight of thelungs but not of other organs in patients dying immediatelyor within 96 h from isolated brain injury. Recently it hasbeen suggested that after acute brain injury there is both anincreased intracranial production of proinflammatory cy-tokines resulting in a secondary injury to the brain [10] andthe release of proinflammatory mediators into the systemiccirculation [11]. Yildirim and coworkers [12] reported thatultrastructural damage occurred in type II pneumocyte ina model of traumatic brain injury, suggesting that an acutesystemic inflammatory response plays an integral role inthe development of such injury by initiating infiltration of
Intensive Care Med (2006) 32:1925–1927DOI 10.1007/s00134-006-0407-z EDITORIAL
Luciana Mascia Ventilatory setting in severe brain injuredpatients: does it really matter?
Received: 18 September 2006Accepted: 18 September 2006Published online: 20 October 2006© Springer-Verlag 2006
This editorial refers to the article available at:http://dx.doi.org/10.1007/s00134-006-0406-0
This work was supported by EEC grants QLCT-2000-00454and QLCT-2002-001160
L. Mascia ()Università di Torino, Dipartimento di Anestesiologia eRianimazione,Ospedale S. Giovanni Battista, Corso Dogliotti 14, 10126 Turin,Italye-mail: [email protected].: +39-011-6335600Fax: +39-011-6960448
Introduction
The presence of pulmonary dysfunction in severe braininjury is a well known phenomenon. Development ofacute lung injury/acute respiratory distress syndrome(ALI/ARDS) occurs in 20–25% of patients with isolatedbrain injury, both subarachnoid hemorrhage and trauma,and is associated with a threefold increased risk of dyingand increased ICU length of stay [1, 2, 3]. IntensiveCareMedicine now present an elegant physiological studycarried out by Koutsoukou and coworkers [4] to assessrespiratory mechanics in the early phase after severebrain injury. The authors conclude that on the first dayof mechanical ventilation patients with brain damageexhibit abnormal respiratory mechanics. Static elastanceand minimal resistance further increased after 5 days inpatients ventilated on zero end-expiratory pressure (ZEEP)
while it remained stable in patients ventilated with a mod-erate level of positive end expiratory pressure (PEEP). Inthe present editorial we discuss: (a) the mechanisms ofpulmonary dysfunction, (b) its clinical relevance, and (c)the potential “conflict of interest” between the protectiveventilation strategy for ALI/ARDS and the ventilatorysettings proposed for brain injured patients.
Mechanisms of pulmonary dysfunction
The risk of developing ALI/ARDS after severe brain in-jury was identified by poorer global initial computed to-mography findings [1] and lower Glasgow Coma Scale [5,6] (intracranial factors) together with the administration ofvasoactive drugs and history of drug abuse (extracranialfactors) [2]. Several mechanisms have been postulated ascauses of pulmonary dysfunction, including aspiration, in-fection, and neurogenic pulmonary edema. In the past theoccurrence of neurogenic pulmonary edema has been at-tributed to a hydrostatic phenomenon induced by a mas-sive increase in sympathetic activity [7, 8, 9]; active pul-monary venocostriction together with an altered capillarypermeability may contribute to an increase in extravascularlung water. Rogers and coworkers [8] confirmed in a largeautopsy database a significant increase in the weight of thelungs but not of other organs in patients dying immediatelyor within 96 h from isolated brain injury. Recently it hasbeen suggested that after acute brain injury there is both anincreased intracranial production of proinflammatory cy-tokines resulting in a secondary injury to the brain [10] andthe release of proinflammatory mediators into the systemiccirculation [11]. Yildirim and coworkers [12] reported thatultrastructural damage occurred in type II pneumocyte ina model of traumatic brain injury, suggesting that an acutesystemic inflammatory response plays an integral role inthe development of such injury by initiating infiltration of
El uso de VT alto se asocia a menor P/F y es predictor
independiente de VALI.
El día 1º los pacientes tienen mala mecánica respiratoria.
Al 5º día con zeep , hay mayor Paw, mayor pCO2, más FR, además de mayor elastancia pulmonar (menor complianza).
1950
paired t test. Regression analysis used the least squaresmethod. Analyses were performed using the softwarepackage Statistica. A p value less than 0.05 was consid-ered statistically significant.
Results
On day 1 FIO2 was 0.46 ± 0.10 in both groups and re-mained essentially constant during the 5-day study period(day 5: 0.45 ± 0.10; Table 3). On day 1 there were no sig-nificant differences in gas exchange or respiratory systemmechanics between the two groups (Table 3). On day 5
Fig.1 The relationship of thechange in minimal resistance ofthe respiratory system(∆Rmin,rs) between days 5and 1 to corresponding changein PaCO2 (∆ PaCO2) in tenbrain-damaged patientsventilated on ZEEP (left) and11 patients ventilated on PEEP(right). All changes refer toabsolute values
PEEP = 0 (n = 10) PEEP = 8 (n = 11)Day 1 Day 5 Day 1 Day 5
FIO2 0.46 ± 0.10 0.45 ± 0.10 0.46 ± 0.10 0.45 ± 0.10PaO2/FIO2 (mmHg) 437 ± 74 346 ± 76* 409 ± 65 331 ± 88*PaCO2 (mmHg) 31 ± 2 34 ± 4* 31 ± 4 33 ± 5DA-aO2 (mmHg) 87 ± 40 123 ± 57 100 ± 41 132 ± 56Est,rs (cmH2O/l) 18.9 ± 3.8 21.2 ± 4.1* 16.1 ± 3.7 18.6 ± 3.3Rmax,rs 9.6 ± 1.9 10.5 ± 2.5 10.9 ± 4.5 10.4 ± 5.2
(cmH2O l− 1s− 1)Rmin,rs 5.6 ± 2.2 6.0± 1.4 5.4 ± 2.5 5.7 ± 4.4
(cmH2O l− 1s− 1)Iso-CO2 Rmin,rs 5.6 ± 2.2 7.0± 1.9* 5.4 ± 2.5 6.5 ± 3.2
(cmH2O l− 1s− 1)∆Rrs 4.1 ± 2.2 4.5± 2.0 5.4 ± 3.2 4.7 ± 1.7
(cmH2O l− 1s− 1)
*p< 0.05, day 5 vs day 1
Table3 Respiratory mechanicsand gas exchange data of the twogroups of patients (FIO2 fractionof inspired oxygen, Est,rs staticelastance of respiratory system,Rmax,rs maximum resistance ofrespiratory system, Rmin,rsminimal resistance of respiratorysystem, iso-CO2 Rmin,rsminimal resistance of respiratorysystem corrected forcorresponding changes in PaCO2
from day 1 to day 5, ∆Rrsadditional resistance ofrespiratory system)
there was a significant PaO2/FIO2 decrease in both groups;in the ZEEP group significant increases in PaCO2, Est,rsand iso-CO2 Rmin,rs (see below) occurred and an almostsignificant increase in DA-aPO2 (p = 0.059). By day 5 onepatient under ZEEP exhibited ALI.
In the ZEEP group there was a significant increasein PaCO2, which is known to affect airway caliber [23].Both on ZEEP and PEEP we found a significant cor-relation between Rmin,rs changes (∆ Rmin,rs) and thecorresponding PaCO2 changes (∆ PaCO2) between days1 and 5 (Fig. 1). When the effects of the PaCO2 changeson Rmin,rs [23] were taken into account using the re-gression models (Fig. 1), on day 5 there was a significant
Intensive Care Med (2006) 32:1947–1954DOI 10.1007/s00134-006-0406-0 OR I GI NAL
Antonia KoutsoukouHelen PerrakiAsimina RaftopoulouNikolaosKoulourisChristina SotiropoulouAnastasia KotanidouStylianosOrfanosCharisRoussos
Respiratory mechanics in brain-damagedpatients
Received: 28 December 2005Accepted: 18 September 2006Published online: 20 October 2006© Springer-Verlag 2006
This article is discussed in the editorialavailable at: http://dx.doi.org/10.1007/s00134-006-0407-z
This work was supported by the Thoraxfoundation.
A. Koutsoukou () ·H. Perraki ·A. Raftopoulou ·N. Koulouris ·C. Sotiropoulou ·A. Kotanidou ·S. Orfanos ·C. RoussosUniversity of Athens, Department ofCritical Care and Pulmonary Services,Evangelismos General Hospital andM. Simou Laboratory, Medical School,45-47 Ipsilandou Street, 10676 Athens,Greecee-mail: [email protected].: +30-210-7201919Fax: +30-210-7216503
Abstract Objective: To assessrespiratory mechanics on the 1stand 5th days of mechanical venti-lation in a cohort of brain-damagedpatients on positive end-expiratorypressure (PEEP) of 8 cmH2O orzero PEEP (ZEEP). Design andsetting: Physiological study withrandomized control trial design ina multidisciplinary intensive care unitof a university hospital. Patientsand measurements: Twenty-oneconsecutive mechanically ventilatedpatients with severe brain damageand no acute lung injury were ran-domly assigned to be ventilated withZEEP (n = 10) or with 8 cmH2Oof PEEP (n = 11). Respiratorymechanics and arterial blood gaseswere assessed on days 1 and day5 of mechanical ventilation. Re-sults: In the ZEEP group onday 1 static elastance and mini-mal resistance were above normallimits (18.9 ± 3.8 cmH2O/l and5.6 ± 2.2 cmH2O/l per second,
respectively); on day 5 static elas-tance and iso-CO2 minimal re-sistance values were higher thanon day 1 (21.2 ± 4.1 cmH2O/l;7.0 ± 1.9 cmH2O/l per second, re-spectively). In the PEEP group theseparameters did not change signif-icantly. One of the ten patients onZEEP developed acute lung injury.On day 5 there was a significant de-crease in PaO2/FIO2 in both groups.Conclusions: On day 1 of mechanicalventilation patients with brain damageexhibit abnormal respiratory mechan-ics. After 5 days of mechanicalventilation on ZEEP static elastanceand minimal resistance increasedsignificantly, perhaps reflecting “lowlung volume” injury. Both couldbe prevented by administration ofmoderate levels of PEEP.
KeywordsMechanical ventilation ·Head injury · Hypocapnic bron-choconstriction ·Ventilator-inducedlung injury
Introduction
A considerable number of patients suffering from severebrain damage require mechanical ventilation during theacute posttrauma phase. Although their morbidity andmortality are caused principally by the primary disease,medical complications are frequent, with respiratory dys-function being the most common nonneurological organsystem failure [1]. In spite of this no study has assessedrespiratory mechanics on the 1st day of mechanical venti-lation in brain-damaged patients. Moreover, although these
patients need prolonged mechanical ventilation becauseof coma and neuroprotection, no study has followed thesepatients to assess whether mechanical ventilation-relatedparameters affect respiratory mechanics.
It has been shown that brain-damaged patients undergoa profound inflammatory response characterized by the re-lease of several cytokines [2] and neuropeptides [3]. Thebiological effects of these substances include leukocyte in-filtration and expression of adhesion molecules [4], bron-choconstriction, mucosal edema, and increased vascularpermeability [5]. There is also evidence that some of these
Intensive Care Med (2006) 32:1947–1954DOI 10.1007/s00134-006-0406-0 ORIGINAL
Antonia KoutsoukouHelen PerrakiAsimina RaftopoulouNikolaosKoulourisChristina SotiropoulouAnastasia KotanidouStylianosOrfanosCharisRoussos
Respiratory mechanics in brain-damagedpatients
Received: 28 December 2005Accepted: 18 September 2006Published online: 20 October 2006© Springer-Verlag 2006
This article is discussed in the editorialavailable at: http://dx.doi.org/10.1007/s00134-006-0407-z
This work was supported by the Thoraxfoundation.
A. Koutsoukou () ·H. Perraki ·A. Raftopoulou ·N. Koulouris ·C. Sotiropoulou ·A. Kotanidou ·S. Orfanos ·C. RoussosUniversity of Athens, Department ofCritical Care and Pulmonary Services,Evangelismos General Hospital andM. Simou Laboratory, Medical School,45-47 Ipsilandou Street, 10676 Athens,Greecee-mail: [email protected].: +30-210-7201919Fax: +30-210-7216503
Abstract Objective: To assessrespiratory mechanics on the 1stand 5th days of mechanical venti-lation in a cohort of brain-damagedpatients on positive end-expiratorypressure (PEEP) of 8 cmH2O orzero PEEP (ZEEP). Design andsetting: Physiological study withrandomized control trial design ina multidisciplinary intensive care unitof a university hospital. Patientsand measurements: Twenty-oneconsecutive mechanically ventilatedpatients with severe brain damageand no acute lung injury were ran-domly assigned to be ventilated withZEEP (n= 10) or with 8 cmH2Oof PEEP (n= 11). Respiratorymechanics and arterial blood gaseswere assessed on days 1 and day5 of mechanical ventilation. Re-sults: In the ZEEP group onday 1 static elastance and mini-mal resistance were above normallimits (18.9± 3.8 cmH2O/l and5.6 ± 2.2 cmH2O/l per second,
respectively); on day 5 static elas-tance and iso-CO2 minimal re-sistance values were higher thanon day 1 (21.2 ± 4.1 cmH2O/l;7.0± 1.9 cmH2O/l per second, re-spectively). In the PEEP group theseparameters did not change signif-icantly. One of the ten patients onZEEP developed acute lung injury.On day 5 there was a significant de-crease in PaO2/FIO2 in both groups.Conclusions: On day 1 of mechanicalventilation patients with brain damageexhibit abnormal respiratory mechan-ics. After 5 days of mechanicalventilation on ZEEP static elastanceand minimal resistance increasedsignificantly, perhaps reflecting “lowlung volume” injury. Both couldbe prevented by administration ofmoderate levels of PEEP.
KeywordsMechanical ventilation ·Head injury · Hypocapnic bron-choconstriction ·Ventilator-inducedlung injury
Introduction
A considerable number of patients suffering from severebrain damage require mechanical ventilation during theacute posttrauma phase. Although their morbidity andmortality are caused principally by the primary disease,medical complications are frequent, with respiratory dys-function being the most common nonneurological organsystem failure [1]. In spite of this no study has assessedrespiratory mechanics on the 1st day of mechanical venti-lation in brain-damaged patients. Moreover, although these
patients need prolonged mechanical ventilation becauseof coma and neuroprotection, no study has followed thesepatients to assess whether mechanical ventilation-relatedparameters affect respiratory mechanics.
It has been shown that brain-damaged patients undergoa profound inflammatory response characterized by the re-lease of several cytokines [2] and neuropeptides [3]. Thebiological effects of these substances include leukocyte in-filtration and expression of adhesion molecules [4], bron-choconstriction, mucosal edema, and increased vascularpermeability [5]. There is also evidence that some of these
Intensive Care Med (2006) 32:1947–1954DOI 10.1007/s00134-006-0406-0 OR I GI NAL
Antonia KoutsoukouHelen PerrakiAsimina RaftopoulouNikolaosKoulourisChristina SotiropoulouAnastasia KotanidouStylianosOrfanosCharisRoussos
Respiratory mechanics in brain-damagedpatients
Received: 28 December 2005Accepted: 18 September 2006Published online: 20 October 2006© Springer-Verlag 2006
This article is discussed in the editorialavailable at: http://dx.doi.org/10.1007/s00134-006-0407-z
This work was supported by the Thoraxfoundation.
A. Koutsoukou () ·H. Perraki ·A. Raftopoulou ·N. Koulouris ·C. Sotiropoulou ·A. Kotanidou ·S. Orfanos ·C. RoussosUniversity of Athens, Department ofCritical Care and Pulmonary Services,Evangelismos General Hospital andM. Simou Laboratory, Medical School,45-47 Ipsilandou Street, 10676 Athens,Greecee-mail: [email protected].: +30-210-7201919Fax: +30-210-7216503
Abstract Objective: To assessrespiratory mechanics on the 1stand 5th days of mechanical venti-lation in a cohort of brain-damagedpatients on positive end-expiratorypressure (PEEP) of 8 cmH2O orzero PEEP (ZEEP). Design andsetting: Physiological study withrandomized control trial design ina multidisciplinary intensive care unitof a university hospital. Patientsand measurements: Twenty-oneconsecutive mechanically ventilatedpatients with severe brain damageand no acute lung injury were ran-domly assigned to be ventilated withZEEP (n = 10) or with 8 cmH2Oof PEEP (n = 11). Respiratorymechanics and arterial blood gaseswere assessed on days 1 and day5 of mechanical ventilation. Re-sults: In the ZEEP group onday 1 static elastance and mini-mal resistance were above normallimits (18.9 ± 3.8 cmH2O/l and5.6 ± 2.2 cmH2O/l per second,
respectively); on day 5 static elas-tance and iso-CO2 minimal re-sistance values were higher thanon day 1 (21.2 ± 4.1 cmH2O/l;7.0 ± 1.9 cmH2O/l per second, re-spectively). In the PEEP group theseparameters did not change signif-icantly. One of the ten patients onZEEP developed acute lung injury.On day 5 there was a significant de-crease in PaO2/FIO2 in both groups.Conclusions: On day 1 of mechanicalventilation patients with brain damageexhibit abnormal respiratory mechan-ics. After 5 days of mechanicalventilation on ZEEP static elastanceand minimal resistance increasedsignificantly, perhaps reflecting “lowlung volume” injury. Both couldbe prevented by administration ofmoderate levels of PEEP.
KeywordsMechanical ventilation ·Head injury · Hypocapnic bron-choconstriction ·Ventilator-inducedlung injury
Introduction
A considerable number of patients suffering from severebrain damage require mechanical ventilation during theacute posttrauma phase. Although their morbidity andmortality are caused principally by the primary disease,medical complications are frequent, with respiratory dys-function being the most common nonneurological organsystem failure [1]. In spite of this no study has assessedrespiratory mechanics on the 1st day of mechanical venti-lation in brain-damaged patients. Moreover, although these
patients need prolonged mechanical ventilation becauseof coma and neuroprotection, no study has followed thesepatients to assess whether mechanical ventilation-relatedparameters affect respiratory mechanics.
It has been shown that brain-damaged patients undergoa profound inflammatory response characterized by the re-lease of several cytokines [2] and neuropeptides [3]. Thebiological effects of these substances include leukocyte in-filtration and expression of adhesion molecules [4], bron-choconstriction, mucosal edema, and increased vascularpermeability [5]. There is also evidence that some of these
Laparotomía descompresiva mejora la PIC en Sd.
Multicompartimental tras TCE.
PIA, la PIC a través de la presión intratorácica.
Resultado de un de la presión intratorácica que provoca
obstrucción al flujo venoso cerebral.
Autorregulación y Vasorreactividad no afectadas por edad,
género, hipo e hiperventilación, hiperoxia y HSA. Leve deterioro en HTA crónica.
Hiperventilación: no recomendada (III). Sólo emergencias con HTIC no controlada. Moderada, limitada.(C)
Hiperoxia: no recomendada.
Seguridad en MRA y VPP-PEEP. Monitorización.
Uso rutinario de PbtO2 como guía terapéutica.
Extubación precoz. Traqueostomia precoz. Destete reglado.
Pensar en el Sd. Compartimental abdominal.
RESUMEN