![]() Cardiac output was measured by transpulmonary thermodilution by injection of 2 ml icecold normal saline into the central venous catheter using a PICCO plus (Pulsion Medical Systems, München, Germany). ![]() ![]() A central venous catheter (3.5 Ch, Tyco, Tullamore Ireland) was introduced into the left femoral vein to measure central venous pressure. A 3F Pulsionkath thermodilution catheter (Pulsion Medical Systems, Munich, Germany) was introduced into the left femoral artery to measure blood pressure, cardiac output and to obtain arterial blood gases. A pulse oximeter (Radical, Masimo, Irvine, CA) was placed on a shaved foreleg. A Stephanie infant ventilator (Stephan, GmbH, Medizintechnik, Gackenbach, Germany) was used throughout the experiments using its calibrated high resolution pneumotachograph. The rate was adjusted to obtain a PaCO 2 in the target range (35–45 mm Hg). During instrumentation animals were ventilated with the following settings: fraction of inspired oxygen: 0.4 tidal volume (V T): 7.5 ml/kg positive end-expiratory pressure (PEEP): 4 cm H 2O inspiratory time: 0.5 sec f = 20/minute. The animals received 5 ml/kg/hr D5 (+70 mEq/L Na +, 18 mEq/L K +). Thereafter, anesthesia was maintained by a continuous infusion of Ketamine (30–100 mg/kg/h) and Xylazine (0.3–1 mg/kg/h). animals were intubated orally with a 3.0 or 3.5 mm cuffed endotracheal tube. Instrumentation and experimental procedureĪfter premedication with atropine 1 mg i.v., Ketamine 15–40 mg/kg i.v. We further explored the effects of different hypercapnia levels on the cardiovascular system in this animal model. We studied the hypothesis, that the reduction of tidal volume to allow for very severe hypercapnia would protect the lung in a “dose”-dependent fashion in this surfactant depletion model for ARDS. In this study we investigated this clinical scenario of down-titration of the tidal volumes in association with progressively high PaCO 2 to evaluate the effects of this strategy on lung injury, gas exchange and on hemodynamics in a controlled established animal model for ARDS. So far, this strategy has to be considered as an experimental approach in individual patient care. This strategy is reserved only for the sickest pediatric ARDS patients and has been used especially in infants and children with respiratory failure after stem cell transplantation that do not qualify for extracorporeal membrane oxygenation therapy. Tidal volumes in these patients often may be well below 5 ml/kg. In adults most recently high levels of hypercapnia associated with hypoventilation are lowered by pump less extracorporeal CO 2 elimination, ,, but so far this not an option for smaller children.Ĭlinically, in infants and children with severe ARDS over the past years we have accepted increasing levels of hypercapnia up to a maximum PCO 2 of 120–140 mm Hg, if necessary to limit peak inspiratory pressures in order to avoid additional lung injury from ventilation. Rather there is a controversy whether associated hypercapnic acidosis caused by hypoventilation should be “permitted” at all and which level of hypercapnia may be acceptable. Nevertheless, in clinical practice therapeutic hypercapnia has not emerged as a concept of therapy. There is some evidence from cell culture and animal studies including our own studies using this surfactant depletion model (unpublished data), that hypercapnic acidosis itself induced by administration of carbon dioxide to the inspired air (so called therapeutic hypercapnia) protects the lung – and increases oxygen delivery to the tissues. Īn increased ventilation rate may allow only to compensate in part for the decrease in tidal ventilation resulting in hypercapnic acidosis. Lower tidal volumes might be more lung protective – but ventilation with too low tidal volumes might increase lung injury by causing atelectasis, increased dead space ventilation, intrapulmonary shunting, hypoxia and hypercapnia –. There is less information on the effects of tidal volumes below 6 ml/kg on the degree of lung injury. The use of low tidal volumes of 6 ml/kg as compared to high tidal volumes of 12 ml/kg decreased the mortality rate of ARDS in adults in the ARDS network trial. Lung protective ventilation strategies in pediatric ARDS include the use of low tidal volumes, avoidance of high peak inspiratory pressures and eventually permission of hypercapnia. Mechanical ventilation is lifesaving in acute respiratory distress syndrome (ARDS), but contributes to lung injury as excessive transpulmonary pressure and alveolar strain lead to formation of alveolar edema, cytokine release from lung endothelial and epithelial cells and infiltration of the lung tissue with granulocytes.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |