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1.
Crit Care ; 16(2): R35, 2012 Dec 12.
Article in English | MEDLINE | ID: mdl-22380702

ABSTRACT

INTRODUCTION: There is mounting evidence that injury to one organ causes indirect damage to other organ systems with increased morbidity and mortality. The aim of this study was to determine the effects of acid aspiration pneumonitis (AAP) on extrapulmonary organs and to test the hypothesis that these could be due to circulatory depression or hypoxemia. METHODS: Mechanically ventilated anesthetized pigs were randomized to receive intrabronchial instillation of hydrochloric acid (n = 7) or no treatment (n = 7). Hydrochloric acid (0.1 N, pH 1.1, 2.5 ml/kg BW) was instilled into the lungs during the inspiratory phase of ventilation. Hemodynamics, respiratory function and computer tomography (CT) scans of lung and brain were followed over a four-hour period. Tissue samples of lung, heart, liver, kidney and hippocampus were collected at the end of the experiment. RESULTS: Acid instillation caused pulmonary edema, measured as increased extravascular lung water index (ELWI), impaired gas exchange and increased mean pulmonary artery pressure. Gas exchange tended to improve during the course of the study, despite increasing ELWI. In AAP animals compared to controls we found: a) cardiac leukocyte infiltration and necrosis in the conduction system and myocardium; b) lymphocyte infiltration in the liver, spreading from the periportal zone with prominent areas of necrosis; c) renal inflammation with lymphocyte infiltration, edema and necrosis in the proximal and distal tubules; and d) a tendency towards more severe hippocampal damage (P > 0.05). CONCLUSIONS: Acid aspiration pneumonitis induces extrapulmonary organ injury. Circulatory depression and hypoxemia are unlikely causative factors. ELWI is a sensitive bedside parameter of early lung damage.


Subject(s)
Pneumonia, Aspiration/physiopathology , Animals , Extravascular Lung Water/metabolism , Heart Conduction System/physiopathology , Hemodynamics , Hippocampus/physiopathology , Hydrochloric Acid , Inflammation/physiopathology , Kidney/physiopathology , Liver/physiopathology , Pneumonia, Aspiration/diagnostic imaging , Pulmonary Edema/etiology , Pulmonary Edema/physiopathology , Pulmonary Gas Exchange , Random Allocation , Statistics, Nonparametric , Swine , Tomography, X-Ray Computed
2.
Neurocrit Care ; 17(2): 281-92, 2012 Oct.
Article in English | MEDLINE | ID: mdl-21647845

ABSTRACT

BACKGROUND: In this study, we compare the effects of high frequency oscillatory ventilation (HFOV) with those of lung-protective volume-controlled ventilation (VCV) on cerebral perfusion, tissue oxygenation, and cardiac function with and without acute intracranial hypertension (AICH). METHODS: Eight pigs with healthy lungs were studied during VCV with low tidal volume (V(T): 6 ml kg(-1)) at four PEEP levels (5, 10, 15, 20 cm H(2)O) followed by HFOV at corresponding transpulmonary pressures, first with normal ICP and then with AICH. Systemic and pulmonary hemodynamics, cardiac function, cerebral perfusion pressure (CPP), cerebral blood flow (CBF), cerebral tissue oxygenation, and blood gases were measured after 10 min at each level. Transpulmonary pressures (TPP) were calculated at each PEEP level. The measurements were repeated with HFOV using continuous distending pressures (CDP) set at TPP plus 5 cm H(2)O for the corresponding PEEP level. Both measurement series were repeated after intracranial pressure (ICP) had been raised to 30-40 cm H(2)O with an intracranial balloon catheter. RESULTS: Cardiac output, stroke volume, MAP, CPP, and CBF were significantly higher during HFOV at normal ICP. Systemic and cerebral hemodynamics was significantly altered by AICH, but there were no differences attributable to the ventilatory mode. CONCLUSION: HFOV is associated with less hemodynamic compromise than VCV, even when using small tidal volumes and low mean airway pressures. It does not impair cerebral perfusion or tissue oxygenation in animals with AICH, and could, therefore, be a useful ventilatory strategy to prevent lung failure in patients with traumatic brain injury.


Subject(s)
Brain/blood supply , Cerebrovascular Circulation/physiology , High-Frequency Ventilation , Intracranial Hypertension/physiopathology , Positive-Pressure Respiration , Animals , Blood Pressure , Cardiac Output , Hemodynamics , Oxygen/metabolism , Pulmonary Gas Exchange , Stroke Volume , Swine , Tidal Volume
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