196,665 research outputs found

    Incidence of intraabdominal hypertension in the intensive care unit.

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    Crit Care Med. 2005 Sep;33(9):2150; author reply 2150-3

    Effect of intra-abdominal pressure on respiratory mechanics

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    Introduction: There has been an exponentially increasing interest in intra-abdominal hypertension (IAH). The intra-abdominal pressure (IAP) markedly affects the function of the respiratory system. Methods: This review with focus on the available literature from the past few years. A Medline and Pubmed search was performed in order to find an answer to the question "What is the impact of increased IAP on respiratory function in the critically ill?". Results: In particular, increased IAP increases chest wait elastance (or decreases compliance) and promotes cranial shift of the diaphragm, with consequent reduction in lung volume and atelectasis formation. Compression of the lung parenchyma also triggers pulmonary infection. During general anaesthesia, in normal subjects, IAP does not affect the chest wait mechanics, but plays a relevant rote in the caudal-cranial displacement of the abdominal content, the diaphragm and consequent changes in lung mechanics and function. In obese patients, the increased IAP is the major determinant of the reduction in lung volume, atetectasis formation and alterations in chest wall mechanics. In ARDS patients the measurement of IAP and chest wait mechanics is important for a better interpretation of respiratory mechanics, hemodynamics and appropriate setting of the ventilator. Furthermore, increased IAP promotes lung oedema, ventilator induced lung injury and reduced lymphatic flow in normal and diseased lungs. Conclusion: Increased IAP markedly affects respiratory function in such a way that it has an impact on daily clinical practise

    Effect of intra-abdominal pressure on respiratory mechanics

    No full text
    Introduction: There has been an exponentially increasing interest in intra-abdominal hypertension (IAH). The intra-abdominal pressure (IAP) markedly affects the function of the respiratory system. Methods: This review with focus on the available literature from the past few years. A Medline and Pubmed search was performed in order to find an answer to the question "What is the impact of increased IAP on respiratory function in the critically ill?". Results: In particular, increased IAP increases chest wait elastance (or decreases compliance) and promotes cranial shift of the diaphragm, with consequent reduction in lung volume and atelectasis formation. Compression of the lung parenchyma also triggers pulmonary infection. During general anaesthesia, in normal subjects, IAP does not affect the chest wait mechanics, but plays a relevant rote in the caudal-cranial displacement of the abdominal content, the diaphragm and consequent changes in lung mechanics and function. In obese patients, the increased IAP is the major determinant of the reduction in lung volume, atetectasis formation and alterations in chest wall mechanics. In ARDS patients the measurement of IAP and chest wait mechanics is important for a better interpretation of respiratory mechanics, hemodynamics and appropriate setting of the ventilator. Furthermore, increased IAP promotes lung oedema, ventilator induced lung injury and reduced lymphatic flow in normal and diseased lungs. Conclusion: Increased IAP markedly affects respiratory function in such a way that it has an impact on daily clinical practise

    Commonly applied positive end-expiratory pressures do not prevent functional residual capacity decline in the setting of intra-abdominal hypertension: a pig model

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    Introduction Intra-abdominal hypertension is common in critically ill patients and is associated with increased morbidity and mortality. The optimal ventilation strategy remains unclear in these patients. We examined the effect of positive end-expiratory pressures (PEEP) on functional residual capacity (FRC) and oxygen delivery in a pig model of intra-abdominal hypertension. Methods Thirteen adult pigs received standardised anaesthesia and ventilation. We randomised three levels of intra-abdominal pressure (3 mmHg (baseline), 18 mmHg, and 26 mmHg) and four commonly applied levels of PEEP (5, 8, 12 and 15 cmH2O). Intra-abdominal pressures were generated by inflating an intra-abdominal balloon. We measured intra-abdominal (bladder) pressure, functional residual capacity, cardiac output, haemoglobin and oxygen saturation, and calculated oxygen delivery. Results Raised intra-abdominal pressure decreased FRC but did not change cardiac output. PEEP increased FRC at baseline intra-abdominal pressure. The decline in FRC with raised intra-abdominal pressure was partly reversed by PEEP at 18 mmHg intra-abdominal pressure and not at all at 26 mmHg intra-abdominal pressure. PEEP significantly decreased cardiac output and oxygen delivery at baseline and at 26 mmHg intra-abdominal pressure but not at 18 mmHg intra-abdominal pressure. Conclusions In a pig model of intra-abdominal hypertension, PEEP up to 15 cmH2O did not prevent the FRC decline caused by intra-abdominal hypertension and was associated with reduced oxygen delivery as a consequence of reduced cardiac output. This implies that PEEP levels inferior to the corresponding intra-abdominal pressures cannot be recommended to prevent FRC decline in the setting of intra-abdominal hypertension

    The effect of non-invasive ventilation on intra-abdominal pressure

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    Background: Non-invasive ventilation is a well-established treatment modality in patients with respiratory failure of different aetiologies. A previous case report described how non-invasive ventilation caused gastric distension and intra-abdominal hypertension with subsequent cardio-respiratory arrest and clinical recovery following resuscitative efforts including gastric decompression with a nasogastric tube. Methods: The aim of this prospective multicentre observational study was to assess the effect of non-invasive ventilation on intra-abdominal pressure. Following informed consent, intra-abdominal pressure and PaCO2were measured before and after the application of non-invasive ventilation for up to three days in critically ill patients requiring non-invasive ventilation. Results: Thirty-five patients were enrolled; mean (±SD) age of 67.8 (±12.5) years, median (interquartile range) body mass index of 27.9 (24.5-30.0) kg m-2, Acute Physiology and Chronic Health Evaluation II score of 15.8 (±6.4). On admission and after 24 hours of non-invasive ventilation, intra-abdominal pressure was 11.0 (7.5-15.0) mm Hg and 11.0 (8.5-14.5) mm Hg (P = 0.82) and PaCO2was 44.4 (±11.4) mm Hg and 51.3 (±14.3) mm Hg (P = 0.19), respectively. Conclusions: The application of non-invasive ventilation was not associated with an increase in intra-abdominal pressure over 72 hours in this small observational study. Thus, it appears that intra-abdominal pressure does not frequently increase when applying non-invasive ventilation in critically ill patients with respiratory failure
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