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Archived Comments for: Effect of a lung recruitment maneuver by high-frequency oscillatory ventilation in experimental acute lung injury on organ blood flow in pigs

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  1. Vital organ blood flow during high-frequency ventilation

    Patrick Meybohm, Department of Anaesthesiology and Intensive Care Medicine, University Hospital SH, Campus Kiel

    29 September 2006

    Patrick Meybohm, M.D.; Jens Scholz, M.D.; Berthold Bein, M.D.

    Department of Anaesthesiology and Intensive Care Medicine, University Hospital Schleswig-Holstein, Campus Kiel, Germany

    We read with interest the article by David et al. [1], comparing the effects of high-frequency oscillatory ventilation with pressure controlled ventilation with respect to vital organ blood flow in an animal model of acute lung injury (ALI). This article provides further information on the issue of interaction between mechanical ventilation and perfusion of different vital organs in patients suffering from ALI. However, there are some points we wish to comment on.

    Firstly, the authors state that their study is limited due to the lack of more frequent blood flow measurements, as all parameters were measured only once thirty minutes after switching to a new mean airway pressure (Pmean), but measurements were performed neither during recruitment manoeuvres (RM) nor repeatedly after RM. Indeed, changes of systemic and cerebral hemodynamic variables are most pronounced straight after increment of Pmean [2]. It has been shown previously, that an increase in positive end-expiratory pressures (PEEP) initially decreased cardiac output (CO) substantially, whereas CO adapted to increased PEEP thereafter due to dynamic hemodynamic changes [3]. Consequently, compensatory mechanisms missed by insufficient data sampling could explain the only slightly decreased CO and mean arterial pressure, and unchanged organ blood flow that did not differ between ventilation modes. Therefore, it is of paramount importance to investigate parameters of systemic and individual organ perfusion more frequently, and obtain variables of both tissue oxygenation and metabolism, such as lactate levels. With respect to short-time effects, impairment of splanchnic circulation during alveolar recruitment with high airway pressures may recover quickly after RM [4], though the consequences of any hypoperfusion regarding bacterial translocation and triggering systemic inflammatory response syndrome in the context of RM have not yet been investigated in a systematic fashion. Contrarily, it is well known that brain tissue is extremely susceptible to ischemia, and even a few minutes of compromised cerebral perfusion affect cerebral metabolic rate of oxygen and tissue integrity. To further elucidate the impact of mechanical ventilation on brain tissue, the authors should have analysed cerebral tissue biochemistry [5] or established traditional biomarkers of cerebral ischemia, such as S-100β or NSE.

    Secondly, the authors chose cardiac filling pressures to represent cardiac preload. These variables, however, have repeatedly been shown to only poorly reflect instantaneous cardiac preload. Specifically, it is well conceivable that hemodynamic effects of RM highly depend on the position of the individual subject on the Frank Starling curve. Therefore, right ventricular end-diastolic volume based on rapid response thermistor technique or global enddiastolic volume obtained by transpulmonary thermodilution would have been more appropriate for this experimental setting. Both have been demonstrated to be clearly superior to cardiac filling pressures particularly at high intrathoracic pressures in a model of ALI [6], and would have provided more detailed information regarding interaction of RM, preload and organ perfusion.


    1. David M, Gervais HW, Karmrodt J, Depta AL, Kempski O, Markstaller K: Effect of a lung recruitment maneuver by high-frequency oscillatory ventilation in experimental acute lung injury on organ blood flow in pigs. Crit Care 2006, 10(4):R100.

    2. Odenstedt H, Aneman A, Karason S, Stenqvist O, Lundin S: Acute hemodynamic changes during lung recruitment in lavage and endotoxin-induced ALI. Intensive Care Med 2005, 31(1):112-120.

    3. Patel M, Singer M: The optimal time for measuring the cardiorespiratory effects of positive end-expiratory pressure. Chest 1993, 104(1):139-142.

    4. Nunes S, Rothen HU, Brander L, Takala J, Jakob SM: Changes in splanchnic circulation during an alveolar recruitment maneuver in healthy porcine lungs. Anesth Analg 2004, 98(5):1432-1438.

    5. Meybohm P, Cavus E, Bein B, Steinfath M, Brand PA, Scholz J, Doerges V: Cerebral metabolism assessed with microdialysis in uncontrolled hemorrhagic shock after penetrating liver trauma. Anesth Analg 2006, 103(4):in press.

    6. Luecke T, Roth H, Herrmann P, Joachim A, Weisser G, Pelosi P, Quintel M: Assessment of cardiac preload and left ventricular function under increasing levels of positive end-expiratory pressure. Intensive Care Med 2004, 30(1):119-126.

    Competing interests