Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

The Open Lung Concept of Mechanical Ventilation: The Role of ...

1,038 views

Published on

  • Login to see the comments

The Open Lung Concept of Mechanical Ventilation: The Role of ...

  1. 1. The Open Lung Concept of Mechanical Ventilation: The Role of Recruitment and Stabilization Ri 陳承勤 2007.04.02
  2. 2. 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
  3. 3. 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
  4. 4. 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
  5. 5. 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.
  6. 6. 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
  7. 7. 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
  8. 8. 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
  9. 9. 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. 
  10. 10. 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
  11. 11. 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
  12. 12. 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
  13. 13. 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
  14. 14. 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
  15. 15. 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-
  16. 16. 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 
  17. 17. 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
  18. 18. 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
  19. 19. 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 
  20. 20. 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
  21. 21. Thanks for your attention!!

×