Brain- Lung Interactions in the Critically Ill

Slide 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

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

Slide 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

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

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

Slide 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

Slide 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

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

Slide 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

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

Slide 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.

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

Slide 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

Slide 14: 2006

Slide 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.

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

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

Slide 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

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

Slide 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

Slide 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

Slide 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

Slide 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

Slide 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

Slide 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

Slide 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