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A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury: Conclusions

The resulting reduction in peripheral oxygen delivery may be counteracted by administration of drugs with positive inotropic action. Such drugs were not given in the present study.
Physiologic dead-space was reduced with PCIRV resulting in an improved alveolar ventilation. This finding is in agreement with previous studies. A reduction of physiologic dead-space seen with prolonged inspiration is usually explained by the occurrence of gas mixing between dead-space and alveolar gas.
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A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury: Gas Exchange

Inverse ratio ventilation tentatively improves recruitment in lung regions with longer time constants (consisting of alveolar units with higher resistance or higher compliance). As a result of smaller airway dimensions, lung units with longer time constants may be more abundant in dependent lung regions. Computer simulations comparing different flow patterns have suggested a more even distribution of ventilation with decelerating flow. However, regional aeration in three vertical zones of the lung were compared and found to be equal between VCV PEEP and PCIRV. There was a tendency toward better aeration with PCIRV in all three zones during dynamic conditions, but the difference was not statistically different.
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A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury: Alveolar Recruitment and Aeration of Lung Tissue

As expected, VCV ZEEP resulted in poorer expiratory aeration in comparison to VCV PEEP and PCIRV. However, no difference in expiratory aeration between the two latter ventilatory modes could be found. The FRC measurements were in agreement with the CT data. These findings indicate that the mechanism for creation of end-expiratory pressure (ie, extrinsic or intrinsic PEEP) is unimportant with respect to the size of increase in end-expiratory lung volume as measured by CT lung density or FRC.
Mean inspiratory lung densities were equal among the three ventilatory modes despite peak airway pressures that were significantly lower with VCV ZEEP and PCIRV than with VCV PEEP.
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A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury: Discussion

However, there were no statistically significant differences between the former two modes, not in static end-inspiration, static end-expiration, or during dynamic conditions (Fig 3).
PaC>2 and venous admixture correlated well to the magnitude of poorly and nonaerated regions (r=—0.87, pCO.OOl, and r=0.88, pCO.OOl) and also to expiratory (r=—0.84, pCO.OOl, and r=0.88, pCO.OOl), inspiratory (r=—0.86, pCO.OOl, and r=0.91, pCO.OOl), and dynamic mean lung density (r=—0.86, pCO.OOl, and r=0.87, pCO.OOl).
FRC correlated closely to expiratory lung density (r=—0.80, pCO.OOl) and also to the difference between expiratory and inspiratory density (r=0.79, pCO.OOl).
There was a greater difference between expiratory and inspiratory lung density in VCV ZEEP than in VCV PEEP and PCIRV (pC0.05). No difference was found between the latter two modes.
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A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury: Computed Tomography

End-expiratory mean lung density during VCV ZEEP (—167 HU) was significantly larger than densities registered during ventilation with VCV PEEP (-333 [pCO.OOl]) and PCIRV (-357 (pCO.OOl). End-expiratory lung densities were equal between VCV PEEP and PCIRV.
Mean lung density at end-inspiration was not significantly different among VCV ZEEP, VCV PEEP, and PCIRV.
Dynamic mean lung density during VCV ZEEP (—260 HU) was significantly larger than densities registered during ventilation with VCV PEEP (—419 HU [pCO.Ol]) and PCIRV (-488 HU [pCO.OOl]). Dynamic mean lung density was equal between VCV PEEP and PCIRV. Figure 1 summarizes the CT density data. purchase antibiotics online

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A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury: Results

Lung injury was characterized by a decrease in static compliance by 12 ml/cm H2O (p<0.05) and by an increase in mean pulmonary artery pressure from 13 to 32 mm Hg (p<0.05). Venous admixture increased from 7 to 45 percent (p<0.05) and PaC>2 fell markedly from 38.7 kPa (290 mm Hg) to 9.3 kPa (70 mm Hg) (p<0.01). Physiologic dead-space increased from 19 percent to 27 percent (p<0.05) and FRC fell from 421 to 207 ml (p<0.05). Table 1 gives a summary of the results.
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A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury: Experimental Protocol

A region of interest (ROI) was constructed by manually delineating the right lung from the chest wall anteriorly, laterally, and posteriorly and from the mediastinal organs medially. Mean density (Hounsfield units, HU) and area (cm2) within the ROI were measured. Poorly aerated and nonaerated lung regions were defined and quantified as areas occupied by voxels between —200 to —100 HU (poorly aerated) and —100 to +100 HU (nonaerated), respectively.
For analysis of regional density, the right lung was divided into three vertical zones of equal height. Within each zone, a ROI was constructed and analyzed for mean density.
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A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury: Hemodynamics

Cardiac output determinations were carried out in triplicate by injecting 10 ml of ice-cold boli of 5 percent dextrose in the right atrium and recording the thermal dilution curve in the pulmonary artery (Edwards Cardiac Output Computer 9520A). Systemic (SAP) and pulmonary artery pressures (PAP) were recorded (Kontron Medical 8A) using pressure transducers (Medex MX807). The pressure registration system was calibrated against a water column and checked prior to each experiment according to standard procedures.
Functional residual capacity (FRC) was determined twice during each ventilatory setting using the sulfur hexafluoride washin-washout technique.
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A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury: Methods

The experimental protocol was approved by the local animal ethics committee.
Twelve pigs weighing 25 ±4 kg were used. After preanesthetic medication with ketamine hydrochloride (10 mg/kg IM), a venous line was inserted into a peripheral vessel and pentobarbital (10 mg/kg) and fentanyl (0.1 mg) were administered. An endotracheal tube (6.5-mm internal diameter) was placed in the trachea through a tracheostomy. The animal was placed in the supine position and the lungs were mechanically ventilated at a respiratory frequency of 15 breaths per minute using a constant inspired oxygen concentration of 60 percent (Siemens Elema Servoventilator 900 C). Minute ventilation was adjusted to obtain normoventilation during baseline recordings prior to lung injury, and was then kept essentially constant throughout the experiment. Anesthesia was maintained by repeated intravenous injections of fentanyl (0.1 to 0.2 mg) and diazepam (0.2 mg/kg) as required. Pancuronium bromide (0.03 mg/kg) in iterated doses was used for muscle relaxation. Throughout the experiment, physiologic saline solution was infused IV at a rate of 100 ml/h other canadianfamilypharmacy.
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A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury

Pressure controlled inverse ratio ventilation A (PCIRV) has been claimed superior to volume-controlled ventilation (VCV) in the treatment of severe acute respiratory failure (ARF). PCIRV has been reported to allow a reduction in minute ventilation, peak inspiratory airway pressure, and externally applied positive end-expiratory pressure (PEEP). Arterial oxygen tension (РаОг) has increased with PCIRV.” It has even been suggested that PCIRV might improve outcome in ARF. However, mean airway pressure increases and cardiac output (CO) falls, the former effect presumed to increase the danger of barotrauma and the latter resulting in reduced oxygen transport to peripheral tissues.
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