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Brain-lung interactions during high-frequency ventilation
- Patrick Meybohm, [Jens Scholz], [Berthold Bein] (27 September 2006)
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Patrick Meybohm University Hospital Schleswig-Holstein, Dept. of Anaesthesiology and Intensive Care Medicine, [Jens Scholz], [Berthold Bein]
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We read with interest the article by David et al.,1 comparing the cerebral effects of high-frequency oscillatory ventilation with pressure controlled ventilation in an animal model of acute lung injury (ALI) and experimental intracranial hypertension (IH). This article provides further information on the issue of interaction between mechanical ventilation and cerebral blood flow in patients suffering from both ALI and elevated intracranial pressure. However, there are some points we wish to comment on. Firstly, all parameters were measured 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. However, changes of systemic and cerebral haemodynamic 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 haemodynamic changes.3 Consequently, compensatory mechanisms missed by insufficient data sampling could explain the unexpected results of unaffected cerebral blood flow (CBF) and sinus sagittalis oxygenation that did not differ between ventilation modes. Therefore, it is of paramount interest to investigate parameters of cerebral circulation more frequently, and obtain variables of cerebral metabolism, such as lactate levels. To further elucidate the impact of mechanical ventilation on cerebral tissue vulnerability, the authors should have analysed cerebral tissue biochemistry4 or established traditional biomarkers of cerebral ischaemia, such as S-100β or NSE. It is well known, that the cumulative time length of compromised cerebral perfusion affects cerebral metabolic rate of oxygen and the risk of cerebral ischaemia. Secondly, the authors chose a model with elevated intracranial pressure. As CBF did not follow decreased cerebral perfusion pressure (CPP), the authors assumed an intact cerebro-vascular autoregulation during their study period. However, patients with IH most often present with impaired cerebro-vascular autoregulation. Therefore, an experimental model with impaired cerebral autoregulation reflecting common clinical scenarios, such as traumatic brain injury or intracerebral haemorrhage, would be more interesting and relevant.5 This is particularly important, since both underlying pathophysiology and behaviour of the cerebral compartment in response to increased Pmean differ. Thirdly, the authors stated that their study is limited due to the lack of CO data. Indeed, CO would have provided more detailed information regarding interaction of RM and organ perfusion. Specifically, it is well conceivable that the lack of differences found with respect to CBF between ventilation modes was due to a differing CO at the time data were obtained. At least during impaired autoregulation cerebral perfusion is closely correlated to CO.6 This may explain, at least in part, why previous studies showed contradictory results with respect to haemodynamic -pulmonary interaction. Finally, the present study did not provide data on intravascular volume. Therefore, the observed severe tachycardia and systemic hypotension may be a result of hypovolaemia, since haemodynamic effects of RM highly depend on the position of the individual subject on the Frank Starling curve. References 1. David M, Markstaller K, Depta AL et al. Initiation of high- frequency oscillatory ventilation and its effects upon cerebral circulation in pigs: an experimental study. Br J Anaesth 2006; 97: 525-32 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: 112-20 3. Patel M, Singer M. The optimal time for measuring the cardiorespiratory effects of positive end-expiratory pressure. Chest 1993; 104: 139-42 4. Meybohm P, Cavus E, Bein B et al. Cerebral metabolism assessed with microdialysis in uncontrolled hemorrhagic shock after penetrating liver trauma. Anesth Analg 2006; 103: in press 5. Lowe GJ, Ferguson ND. Lung-protective ventilation in neurosurgical patients. Curr Opin Crit Care 2006; 12: 3-7 6. Bein B, Meybohm P, Cavus E et al. A comparison of transcranial Doppler with near infrared spectroscopy and indocyanine green during hemorrhagic shock: a prospective experimental study. Crit Care 2006; 10: R18 Conflict of Interest:None declared |
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