Pathophysiology of mechanical ventilation cairo program dec 2011

Pathophysiology of Mechanical Ventilation PJ Papadakos MD FCCM FCCP Director CCMProfessor Anesthesiology, Surgery and Neurosurgery University of Rochester School of Medicine Rochester NY Professor Respiratory Care State University Of New York Genesee Community College Batavia NY

20 year collaboration Rotterdam and now Berlin

Funding over the Years:SiemensErasmus UniversityEuropean UnionBerlin UniversityAstra ZenecaBOCLilly

The Facts on Mortality

Dept. of Anesthesiologymortality rate (%) Mechanical ventilation overall ventilated ARDS Esteban et al. JAMA 2002; 287

Dept. of AnesthesiologyNinety-day mortality10080 41.3% 44.2%604020 0 non-ARDS ARDS Luhr et al. Intensive Care Med 2000: 26:508-17

Basic PhysiologyThe Base of Good Care In all trauma patients

What do these have in common

ARDS NetShowed that we are mammals!

Lung Skeleton

Lung Skeleton  Force-bearing structure  Elastin and collagen that are embedded in a the extracellular matrix  Two fiber systems connected at alveolar levels one originating from the hilum and the other from the visceral pleura in the peripheryPapadakos, Karcz and Lachman Mechanical Ventilation in Trauma, Curr Opin inAnesthesiol 23 2010

Microstructure

The Breathing Muscle It Goes up andDown

Chest Expansion Generating Flow

Change in muscle fibers Type I Type IIa Type Iid/x Type IIb Slow Fast Fast Fast Shanely et al. AJRCCM 2002;166:1369-74

Controlled mechanical ventilation Powers et al. JAP 2002;92:1851-8

St. Michael’s Hospital A teaching hospital affiliated with the University of TorontoLevine et al. NEJM 2008; 358:1327-35

47 Days 3 Days Knisely et al. J Pediatric 1988;113:1074-7

Physiology of Atelectasis

Fact !Each lung hasa tendency to collapse

Decreased Oxgenenation

Eskaros and Papadakos Respiratory Monitoring in Millers Anesthesia 7th

Lung Mechanics change with Lung Collapse

Shear Forces

VOLUTRAUMA trauma fromhigh lung volumes ATELECTRAUMA (RACE) trauma from low lung volumes

Pulmonary Surfactant

Surfactant 90% lipids 10% ProteinsHydrophilic: SP-A and SP-DHydrophobic: SP-B and SP-C

Curr Opin Crit Care 10, 2004: 18-22

Pulmonary Surfactant wasinitiallyidentified as a lipoproteincomplex that reducessurface tension at the air-liquid interface of the lung

Lipids Levels of total phospholipids decrease over time with cyclic opening and closing especially phosphatidylcholine and phosphatidylglycerol, which are essential for lowering surface tension at the alveolar capillary membrane.Tsangaris l. et al Eur Respir J 2003, 21:495-501

The cycle opening andclosing of AlveolarUnits Deplete Surfactant and lead tofurther collapse through clumping.

Key to Immunology And host defence

Lung host defence mechanisms the lung is constantly challenged by inhaled pathogenPollutants an particles

of a family of proteins known as collectins.

Surfactant Proteins A and SP-D potentially bind several receptors, including Toll receptors

SURFACTANT INACTIVATION DECREASED SURFACTANT ACTIVITY HIGH INCREASEDPERMEABILITY SURFACE TENSION EDEMA AT ALVEOLAR WALL INCREASED SUCTION FORCES ACROSS ALVEOLAR WALL

Cascade of cytoactive molecules

From our Lab in Rotterdam:

Dept. of Anesthesiology Ventilator-associated lung injuryPurine conc BALF (M) 4 3 2 1 0 Surfactant Control 7/0 45/10 45/0 Verbrugge et al. Crit Care Med

Effect of ventilation on renal 100 failure% of renal failure entry 75 72-96 h 50 535.9 507.2 280.1 25 14 86 18 18 0 Conventional Protective ventilation ventilation (n=22) (n=22)

Effect of ventilation on hepatic failure% of hepatic failure 40 entry 30 72-96 h 20 535.9 507.2 280.1 10 0 23 9 5 0 Conventional Protective ventilation ventilation (n=22) (n=22)

A Systemic Inflammatory Process

Nosocomial Pneumonia

Medicare and Insurance Guidelines

Nosocomial Pneumonia Head of Bed Up Suctioning Mouth and Subglotic Mouth Care Oral intubation and Special ET tubes Hand washing and gowns Low gastric volumes Humidification

Presence of atelectasis Leads to impairment of host defense promotes nosocomial pneumonia

Nosocomial Pneumonia True Protection

Many Things Do Not Work

Critical Care Medicine 36, #3: 782-788 2008

Lets Jump into some up coming ideas on ventilation

Dept. of Anesthesiology Surfactant Depletion followed by 4 hrs of Mechanical ventilation P/F-ratio: P/F -Ratio: 310 650© B. Lachmann Open Lung Strategy ARDS Network Protocol

ARDSnet PermissivePEEP table = atelectasis M.Amato

PermissiveAtelectasis

PermissiveARDSnetatelectasis

PermissiveAtelectasis

PermissiveARDSnetatelectasis

PROTETORA Open Lung

Regional Spectrum of Opening Pressures Opening Superimposed Pressure Pressure Inflated 0 Small Airway 10-20 cmH2O Collapse Alveolar Collapse 40-60 cmH2O (Reabsorption) Consolidation (modified from Gattinoni)

PEEP Is natural It keeps recruited units open Must be titrated

Dept. of Anesthesiology Healthy Tween Tween & PEEP© B. Lachmann Steinberg et al. Am J Respir Crit Care Med; 2004; 169: 57-63

Dept. of AnesthesiologyPEEP levels used in patients on mechanical ventilation: international data 50 40 Patients (%) 30 20 10 0 0 1 to 5 6 to 10 11 to 15 >15 PEEP (cm H2O) Esteban et al. Am J Respir Crit Care Med 2000:161:1450-8

Barbas et al. Am J Respir Crit Care Med; 2002,

Hamdan A. A , Papadakos PJ Saunders Manual of Critical Care 2002

Small Positive End-Expiratory Pressure Decrease Results in Dramatic Pa02 ChangesIn a Experimental Model of ARDSSchwaiberger, Lachmann,Papadakos and LeonhardtATS 2011

1998,VOLUME 338 February, 5 NUMBER 6 NUMBER 6

Survival function - Amato et al. 1.0Cumulative Survival .8 Protective .6 P < 0.001 .4 Control .2 N = 53 0.0 0 10 20 30 Time after Entry ( days )

Many ThanksTo my many Friends

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Pathophysiology of mechanical ventilation cairo program dec 2011

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