High Frequency Oscillatory Ventilation

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Presentation transcript:

High Frequency Oscillatory Ventilation Bradley Fuhrman, MD Professor and Chair, Department of Pediatrics brad.fuhrman@ttuhsc.edu COI – but will not discuss: Royalty Cook Catheter Equity Medical Conservation Devices

HFOV is a lung protective strategy. The natural history of acute respiratory failure is influenced by the way the lung is ventilated. The cardinal feature of Ventilator Induced Lung Injury (VILI) is pulmonary edema formation.

Effects of High Pressure Ventilation Normal, 5 min @ 45 cm H2O, 20 min @ 45 cm H2O (Dreyfuss and Saumon)

Over-Distension Pulmonary Edema Is Protein Rich

Alveolar wall tension stretches alveolar capillaries - especially corner vessels…

Increased Wall Tension Raises Transmural Pressure Across Corner Vessels Interstitial Pressure Capillary Pressure Corner Vessel Alveolar Septum High lung volume and high surface tension promote transudation.

Traction on capillaries causes endothelial cell disruption. allows PMNs to contact basement membrane PMNs accumulate after several hours of VILI

Biotrauma Neutrophil accumulation Neutrophil activation Cytokine elaboration Inflammation Increased capillary permeability to water, albumin and other proteins

Surfactant dysfunction or deficiency lowers the pressure surrounding pulmonary capillaries and promotes fluid flux. Proteases that leak into alveoli with edema fluid inactivate surfactant.

Mechanisms of VILI Increased vascular transmural pressure causes transudation of fluid Surfactant dysfunction promotes capillary filtration Direct trauma causes permeability edema Biotrauma and inflammation promote capillary permeability and oxidative injury to cell membranes and other cell components

Mechanisms of VILI Increased vascular transmural pressure causes transudation of fluid Surfactant dysfunction promotes capillary filtration Direct trauma causes permeability edema Biotrauma and inflammation promote capillary permeability and oxidative injury to cell membranes and other cell components

Mechanisms of VILI Increased vascular transmural pressure causes transudation of fluid Surfactant dysfunction promotes capillary filtration Direct trauma causes permeability edema Biotrauma and inflammation promote capillary permeability and oxidative injury to cell membranes and other cell components

Mechanisms of VILI Increased vascular transmural pressure causes transudation of fluid Surfactant dysfunction promotes capillary filtration Direct trauma causes permeability edema Biotrauma and inflammation promote capillary permeability and oxidative injury to cell membranes and other cell components

Which clinical choices promote or avoid VILI ?

Volutrauma vs Barotrauma High Vt, Paw=0 Negative Pressure Vent High Vt, High Paw Positive Pressure Vent Thoracoabdominal- Strapped High Pressure Low Vt VILI can occur at high lung volume despite low airway pressure…

Upper Inflection Point – Over-distension (Dreyfuss) Lower Inflection Point – Opening/Closing Alveoli (Slutsky) Upper Inflection Point Lower Inflection Point Lung Volume Static Airway Pressure

Open Lung Strategy to Avoid VILI PEEP > LIP Pplateau < UIP Amato et al (1995)

NIH ARDS Network Trial (PEEP not controlled) 6ml/kg vs 12 ml/kg low TV 30% Mortality high TV 40% Mortality

HFOV as an Open Lung Strategy

Inspiration Piston Bias Flow Mushroom Exhaust Valve

Expiration Piston Bias Flow Mushroom Exhaust Valve

Piston Forward MAP Piston Back

Inspiration x x x xxx xxx xxx xx xxx x xxx xxx x xxx xxx xx

Expiration x xxx xx xxx xxx xxx xxx xx xx

Mary Ellen Avery: “It’s like stirring your coffee after you add cream

Open Lung Strategy – Lung Protective Indications for HFOV Open Lung Strategy – Lung Protective A Rescue Strategy Excessive Peak Pressure (Above UIP) Air Leak at High Peak Airway Pressure Very Low FRC Requiring High Airway Pressure to Maintain Oxygenation Very low Compliance Limiting TV - Causing Hypercarbia Cardiac Output Impaired by High Peak Airway Pressure

How to Use HFOV in an Open Lung Strategy Set mean airway pressure between LIP and UIP Assure Oxygenation Increase amplitude until CO2 clearance becomes adequate

Setting MAP Open Lung Strategy Generally start 5 to 7 cm H2O above MAP on conventional mechanical ventilation Increase as needed to achieve desired oxygenation May be limited by effect on cardiac filling MAP is set by adjusting pressure at which mushroom valve opens.

Setting Amplitude Amplitude impacts pCO2 TV proportional to amplitude Amplitude set by adjusting power (piston excursion) Reading of amplitude is before endotracheal tube Should see jiggle at thighs

Pressure amplitude is dampened by Endotracheal Tube.

Setting frequency Generally 3 to 6 Hz in adults Optimal Hz is inversely proportional to weight Reduce frequency to improve CO2 clearance

Optimal Tidal Volume ~ 2 ml/kg Not Measured

Setting bias flow In expiration, as piston moves back, expired air enters oscillator tubing In early expiration may move both toward mushroom and toward piston In late expiration, with mushroom closed, expired air can only move toward piston Bias flow flushes gas in oscillator to eliminate CO2 Toward patient and mushroom in inspiration Toward piston in expiration

Piston Forward MAP Bias Flow Piston Back

Proof of Efficacy FDA approval based on avoidance of ECMO in MAS Arnold et al 1994 – Better oxygenation, less barotrauma… Bohn et al 1999 – Rev – No improvement in outcome… Derdak et al 2001 – RCT – Safe and effective in adults… Ritacca et al 2003 – Rev – As good as CMV…

Thank you…