The Open Lung Concept of Mechanical Ventilation: The

Role of Recruitment and Stabilization

Ri 陳承勤2007.04.02

Overview Introduction The physiology and pathophysiology of

mechanical ventilation Modes of ventilation that will prevent

ventilation -induced lung injury Pressure-controlled ventilation The open lung concept (OLC) Conclusion

Introduction A key measure of patient outcome and

the quality of care in ICU is ventilator-free days.

Ventilatory protocols for acutely ill patients in the ICU has been improving continually.

Strategies have changed from optimizing convenient physiology variables, such as O2 and CO2 levels, to protecting the lung from injury and↓cytokine modulation of the lung

Introduction The strategy of lung recruitment or

open lung concept (OLC) refers to the dynamic process of opening previously collapsed lung units by ↑transpulmonary pressure.

The OLC may play an important role in preventing ventilator-induced lung injury

This article describes the pathophysiologic basis and clinical role for lung recruitment maneuvers.

The physiology and pathophysiology of mechanical

ventilation ↓lung distensibility is a disturbed

surfactant system ↑surface tension (T) ↑forces

acting at the air–liquid interface the end-expiratory collapse, atelectasis,↑right to left shunt, and↓PaO2.

Two primary mechanisms of surfactant failure related to mechanical ventilation have been described.

The physiology and pathophysiology of mechanical

ventilation In the first mechanism, mechanical

ventilation enhances surfactant release from the pneumocyte type II into the alveolus, lost into small airways due to compression of the surfactant film.

The changes in alveolar surfactant may affect the permeability of the alveolocapillary barrier to small solutes and proteins ↑pulmonary leak

in respiratory failure and the formation of edema.

The physiology and pathophysiology of mechanical

ventilation Surfactant composition and function can

be impaired by inhibitory factors from protein- rich pulmonary edema fluid or by the degradation in the alveolar space due to lipases and proteinases

The second mechanism is that the alveolar surfactant and the changes that are associated with mechanical ventilation may result in the conversion of surface-active, large surfactant aggregates into nonsurface-active aggregates

The physiology and pathophysiology of mechanical

ventilation Surfactant changes caused by

mechanical ventilation are reversible due to a metabolically active de novo production of surfactant.

The barrier function of surfactant may collapse with mechanical ventilation, and there may be transmigration of bacteria.

High-peak inspiratory lung volumes +↓positive end-expiratory pressure (PEEP) ↑proinflammatory mediators from the lung tissue into the airway.

The physiology and pathophysiology of mechanical

ventilation 10 cm H2O of PEEP at comparable

peak inspiratory lung volumes or lowering peak inspiratory lung volume when ventilating with zero PEEP reduced these cytokine levels .

Lung, an important causative part of an inflammation-induced systemic disease state MOF,not only a pulmonary disease process.

Alveolar collapse with improper mechanical ventilation(↓PEEP↑VT) activation of SIRS

Modes of ventilation that will prevent ventilation-induced lung

injury The standard physiologic tidal volume

of 5 to 7 cc/kg had been adopted The common practice of an unnatural tidal

volume of over 10 cc/kg was wrong. The authors are hopeful that this natural

tidal of 5 to 7 cc/kg has been accepted into practice and is common practice in all ICUs.

This simple change in practice will contribute greatly to the outcome of ventilated patients.

Pressure-controlled ventilation Artificial ventilation direct lung damage

and modulate cytokine release Atelectasis not only affects local gas

exchange but also affects nonatelectatic areas.

The cycle of continuous expansion and collapse of alveoli in respiratory cycle structural changes by barotrauma and volutrauma, as well as surfactant function and cytokine release

Pressure-controlled ventilation High opening pressure to recruit

the lung and lower pressures to keep the alveoli open

In normal lung, alveolar surfactant ↓surface

forces of the air–liquid interface alveolar stability at all alveolar sizes .

In ventilated lungs, varied levels of surfactant system dysfunction due to either direct ventilator effects or indirect effect of the systemic inflammatory response.

Pressure-controlled ventilation The degree of this surfactant dysfunction

will determine the amount of pressure needed to expand alveoli from closed to open.

Pressure-controlled ventilation control ventilatory pressure necessary to expand alveoli.

In true alveolar collapse, the pressure needed for

alveolar recruitment may reach above 70 cmH2O

Alveolar bed may be opened best using the decelerating wave pattern of pressure control

Pressure-controlled ventilation A concept of pressure-control ventilation

is fresh gas distribution in the lung. A decelerating pattern opens alveoli

better than a constant flow pattern When new alveoli recruited,volume

necessary to fill the alveoli from ventilator, source

of higher pressure, not from adjacent lung

units,because there is equal pressure in all areas of the

lung

Pressure-controlled ventilation ↓alveoli size flow of fresh gas from

highest pressure, always ventilator into

alveoli unit better gas exchange Volume control intrapulmonary

redistribution of gas from other hyperdistended lung

units,so- called Pendelluft effect. Pressure-control no redistribution

only fresh as is entering the recruited alveoli

The open lung concept ARDS multiple atelectasis, % of

recruitable lung varied widely, from negligible to >50%

The treatment for alveolar collapse is lung recuitment, the open lung concept (OLC)

In healthy lungs, % of recruitable lung close

to zero because normal function surfactant

maintains alveolar units in a noncollapse status

The goal of OLC ↓collapse atelectasis and

↑optimal gas exchange

The open lung concept ↑initial inspiratory pressure recruit

collapse alveoli, then minimal pressure prevent

lung from collapsing Intrapulmonary suction renewed

collapse of alveoli PaO2↓,secretion management must be balance with alveolar recruitment

Early OLC ( < 72hrs ) higher response rate, this probably related to the change from exudate to a fibroproliferative process

The open lung concept OLC may be applied in at-risk patient

during Sx Recruitment at early stage of severe lung

injury dramatically improve oxygenation and

maintain the newly recruited lung tissue The peak inspiratory pressure (PIP) is

adjusted to the lowest pressure, which keep the lung

open. The ideal pressure is 15~30 cmH2O

to prevent alveolar collapse.

Conclusion and take home message

Lung recruitment opening collapsed lung units by↑transpulmonary pressure (PA-Ppl).

↓PEEP↑VT continuous expansion and collapse of alveoli barotrauma + volutrauma, surfactant dysfunction and cytokine release activation of SIRS

High PEEP ↓cytokine level. Standard physiologic VT 5 to 7 cc/kg

Conclusion and Take home message

High opening pressure to recruit the lung and lower pressures (PEEP) to keep the alveoli open

The ideal pressure is 15~30 cmH2O to prevent alveolar collapse.

Pressure-control fresh gas from ventilator, higher pressure, not from adjacent lung units

Volume control intrapulmonary redistribution of gas Pendelluft effect.

ARDS multiple atelectasis, % of recruitable lung varied widely, from negligible to >50%

Thanks for your attention!!