Presentation of Dr. Lluis Blanch at 8th Pulmonary Medicine Update Course, February 2008, Cairo, Egypt. Pulmonary Medicine Update Course is organized by Scribe : www.scribeofegypt.com

1. 8th Pulmonary Medicine Update Course
The Egyptian Society of ICM & Trauma
Brain-Lung Interactions in
the Critically Ill
Lluis Blanch M.D.
Consultant, Critical Care Center, Hospital of Sabadell
Scientific Director, Corporacio Parc Tauli
University Institut Fundació Parc Taulí
Universitat Autónoma de Barcelona
Sabadell, Spain
lblanch@tauli.cat
Cairo, February 6 - 7, 2008

2. Does Distant Organ Injury -Brain- Render the
Lung More Susceptible to Mechanical Injury ?

3. European Journal of Cardio-Thoracic Surgery 25 (2004) 523-529
Intracellular vacuoles
Interstitial & mitocondrial edema
Dilatation in endoplasmic reticulum & Golgi
Chromatin desintegration in the nucleus
G5
2h 8h 24h

4. These data strongly support that a secondary
lung inflammatory response may develop
immediately following intracerebral hemorrhage

5. BALF
Rats with TBI
Contusion:
Mild to
Moderate
TBI
BALF

6. Massive Brain Injury
Catecholamine
Storm Brain Ischemia
Hypertensive Hemodynamic Inflammatory
Crisis & Changes Mediators
Neurogenic
Hypotension Organ
Hydrostatic
Ischemia
Sympathetic Pressure
Alteration of
Capillary Blood-Gas Endothelial Stretch
Permeability Barrier Damage & Shear Stress
Neurogenic Pulmonary Edema & Acute Lung Injury

7. Hemodynamic Mechanisms of Lung Injury & Systemic Inflammatory
Response Following Brain Death in the Transplant Donor
Methods: Control & Brain Death rats
α
Interventions: Elimination of the hypertensive response (α-adrenergic
antagonist) & Correction of hypotension (noradrenaline)
*
*
Serum BAL 4 h.
*
*Rupture of the capillary-alveolar membrane at 4 hours
Avionitis VS et al. Am J Transplantation 2005; 5:684-693

8. Crit Care Med 2005;33:1077-83

9. Isolated Heart-Lung Block
ex - vivo period: 30 minutes
Control & Massive
Brain Injury Groups:
PCV 30 cmH2O
PEEP 5 cmH2O
Blood Flow 300 ml/min
LAP 10 mmHg

10. Crit Care Med 2005;33:1077-83
Weight
Massive Brain
Injury
Weight (gr)
Control
Time (sec)

11. Brain Signaling
during Systemic Inflammation
Systemic Inflammation
Brain Activation
(antiinflammatory response)
Brain Damage
(excess of pro-antiinflammatory mediators)
Neuroimmune Comunication with Intact
Blood Brain Barrier Occurrs at:
- Circumventricular organs
- Activity in vagus nerve
Ebersoldt M et al. Intensive Care Med 2007;33:941-50
Sharshar T et al.Crit Care 2004;8.

12. S-100: cerebral
specific marker
Lung Injury
Hypoxia-only
Acute lung injury leads to
neuropathologic changes
independent of hypoxemia

13. Prevention of Secondary Ischemic
Insults after Severe Head Injury
n = 189 ARDS more frequent in
CBF-targeted protocol
ICP-targeted protocol:
- CPP > 50 mmHg
- PaCO2 25-30 mmHg
CBF-targeted protocol:
- CPP > 70 mmHg
- PaCO2 35 mmHg
Robertson CS et al. Crit Care Med 1999; 27: 2086-2095

14. 2006

15. Crit Care Med 2006;34:321-7
Standard ventilatory managenent in 34 potential donors
Histograms of VT & PEEP
Data show that 45% of potential lung donors had PaO2/FIO2 ratios
= or < 300 mmHg, rendering them ineligible for lung donation.

16. +
Normocapnia Moderate Hypercapnia
& &
CPP > 60 mmHg Moderate / High PEEP
VILI ↑ CBF & ↑ ICP
ALI / ARDS Secondary Brain Injury

17. Brain Injury & Respiratory Failure
Targets during MV:
To protect the brain & the lung
Aim:
Reduction of lung injury & prevention
of brain injury amplification

18. Carbon Dioxide & Cerebral Circulation
in Patients with Severe Head Injury
PaCO2 PaCO2
Hypercapnia causes vasodilation Hypocapnia causes vasoconstriction
and reduction of cerebral vascular with a subsequent reduction in CBV,
resistance with a subsequent leading to a reduction in ICP
increase in CBF & CBV
High PaCO2-induced
dilatation of cerebral
Intracellular pH that normalizes in hours
resistance vessels
Extracellular pH that normalizes in 1-2 d.
depends on pHe
ICP
Brian J. Anesthesiology 1998;88:1365. Stocchetti N et al. Chest 2005;127:1812.
Laffey JG & Kavanagh BP. Permissive Hypercapnia. In Tobin MJ. 2006

19. J Trauma 2007;62:1330-8
Crit Care Med 2006;34:1202-8
Odds Ratio
of Survival

20. Effects of Varying Levels of PEEP on ICP
and Cerebral Perfusion Pressure
Normal ICP Elevated ICP
McGuire G et al. Crit Care Med 1997;25:1059-1062
ICP & PEEP Interactions:
1. Waterfall theory: the highest ICP, the lower impact of PEEP
2. Airway pressure transmission to vessels: lung & chest wall
3. Abdominal and spinal compartments

21. 12 severely brain-injured patients with ALI & ICP higher
than applied PEEP. Interventions: PEEP 5 & 10
25 25
PaCO2
(%)
-60 80 -40 80
-10 -10
C Est,rs (%)
Est,rs (%) ICP (%)
Recruiters Non-Recruiters

22. Physiologic Effects of Tracheal Gas Insufflation
TGI: Dilute the CO2 that remains in
the anatomic & apparatus dead space Control Phasic TGI
Blanch L, Nahum A. Transtracheal Gas Insufflation. In: Principles & Practice
of Mechanical Ventilation. Tobin M, ed (2nd ed). McGraw-Hill 2006

23. 7 patients with Severe Head Trauma (GCS < 9) & ALI/ARDS
Basal-pre TGI Basal-post
P/FiO2 mmHg 151 ± 45 164 ± 35 174 ± 34
VT ml/kg 9.1 ± 0.8 7.2 ± 0.7 9.1 ± 0.8
VE L/min 11.8 ± 2.9 9.2 ± 2.1 11.7 ± 3.0
PEEP tot cmH2O 9.3 ± 2.8 12.7 ± 3.4 9.5 ± 2.6
Drive Paw cmH2O 18.1 ± 3.4 13.2 ± 2.1 16.7 ± 3.5

24. Basal-pre TGI Basal-post
PaCO2 mmHg 36 ± 1 36 ± 1 36 ± 1
ICP mmHg 19 ± 6 19 ± 5 17 ± 4
CPP mmHg 76 ± 11 79 ± 11 74 ± 10
SjO2 % 72 ± 9 73 ± 9 71 ± 10

25. Supine Prone
51 pats.
• Similar incidence of death,
duration of MV and neurologic
outcome.
• PP reduced the incidence of lung
worsening.
• Less episodes of VAP in PP group
(20%) compared to Supine (38.4%)
• In PP group significant increase in
intracraneal pressure

26. Tips to Ventilate Patients with
Brain & Lung Injury
Minimize alveolar overdistension during inspiration:
Pplat < 30 cmH2O, VT < 8 ml/kg
Minimize alveolar de-recruitment during expiration:
moderate, high PEEP
Minimize instrumental dead space
Optimize respiratory rate
Monitor respiratory (SpO2, etCO2, IAP, Pplat, total PEEP, Crs) and
brain variables (ICP, TC doppler, SjO2) to reset the ventilator
according to them.
Prone position in most severe ARDS but early