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PubMed1987

Jet ventilation in support of fiberoptic bronchoscopy.

Mechanical ventilatory support of bronchoscopic procedures by conventional volume-cycled ventilation (VCV) is technically difficult and can result in unreliable gas delivery or excessive alveolar pressure. An alternate support mode is jet ventilation through an open, uncuffed endotracheal tube. To quantitate gas delivery and airway pressures (Paw) during bronchoscopy using this technique, we used a mechanical-lung model and 15 human subjects. Jet ventilation pulsed gases at 60 to 100 cycle/min through a catheter in an uncuffed, jet endotracheal tube with a 5.9-mm (OD) bronchoscope in place. Inspiratory time was constant at 33% of cycle time, and jet-drive pressures ranged from 5 to 30 psi. In the mechanical-lung model, the jet technique provided up to 30 L/min of ventilation with mean airway pressures (Paw) always less than 10 cm H2O. In contrast, VCV with an inflated cuff, while providing similar levels of ventilation, resulted in substantial air trapping and over twice the Paw. VCV with a deflated cuff provided much lower levels of ventilation, although Paw levels were also low. These delivered minute ventilations, and Paw levels were similar in six normal volunteers jet ventilated through a 9-mm jet endotracheal tube with a bronchoscope in place. Finally, in nine patients requiring mechanical ventilatory support during bronchoscopic procedures, this jet technique provided alveolar ventilation (i.e., PaCO2) and Paw levels comparable to those obtained on baseline VCV before bronchoscopy.

Adult↗
PubMed1987

A technique for the administration of ribavirin to mechanically ventilated infants with severe respiratory syncytial virus infection.

Fifteen infants with respiratory syncytial virus pulmonary infection admitted to our pediatric ICU from December 1, 1985 through April 30, 1986, required mechanical ventilation. These patients were placed on an open trial of ribavirin therapy. We describe a technique for the safe delivery of aerosolized ribavirin to these infants while on the ventilator. The agent was delivered for 16 h/day for 7 days. Modifications of the ventilator circuit were needed to prevent the condensation of the drug in the ventilator tubing and to allow for the safe and effective operation of the ventilator. A common ventilator strategy was used for all patients. The highest positive inspiratory pressure generated was 42 +/- 9.5 (SD) cm H2O, the highest PEEP was 5.9 +/- 3.2 cm H2O, the duration of ventilation was 10.7 +/- 8.5 days, and exposure to fraction of inspired oxygen was greater than or equal to 0.6 for 55.3 h. Ribavirin levels were measurable in two patients, thereby demonstrating that the drug was in fact delivered and absorbed. Our preliminary results demonstrate that ribavirin can be delivered to the patients with respiratory syncytial viral infections who require mechanical ventilation; however, further studies are indicated to evaluate the efficacy and dose responsiveness, alterations in pulmonary dynamics, and safety of ribavirin in delivery to infants requiring ventilation.

Administration, Inhalation↗
PubMed1997

Effects of prolonged controlled mechanical ventilation on diaphragmatic function in healthy adult baboons.

OBJECTIVE: To study diaphragmatic strength and endurance after a prolonged period of mechanical ventilation. DESIGN: Prospective animal study. SETTING: Animal research laboratory. SUBJECTS: Seven uninjured adult baboons (Papio cynocephalus) were anesthetized with ketamine, sedated, paralyzed, and mechanically ventilated. Animals were monitored with pulmonary arterial and peripheral arterial catheters. INTERVENTIONS: Mechanical ventilation was provided for 11 days with an FIO2 of 0.21 and tidal volume of 15 mL/kg. Pulmonary function tests, including lung volumes, arterial blood gases, and chest radiographs were also monitored. Nursing care procedures included frequent turning, chest physiotherapy, and endotracheal suction. Antacids and prophylactic antibiotics (intravenous penicillin, topical polymyxin B, and gentamicin sulfate) were administered. In three animals, fishhook electrodes were surgically placed around both phrenic nerves on both day 0 and after 11 days of mechanical ventilation for diaphragmatic stimulation. On day 0, the electrodes were removed after phrenic nerve stimulation studies were performed. After 11 days of mechanical ventilation, animals were electively killed and full autopsy performed. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and pulmonary function parameters were measured at baseline and every day during the 11 days of mechanical ventilation. Diaphragmatic strength and endurance were measured on days 0 and 11. Diaphragmatic endurance was determined by an inspiratory resistive loading protocol. There were no significant changes in hemodynamics, lung volumes, or gas exchange during the period of mechanical ventilation. On day 7, the chest radiographs showed patchy lobar atelectasis in six animals, which cleared by day 11 in all but two of the animals. Lung pathology showed mild, focal pneumonitis. By day 11, maximum transdiaphragmatic pressure had decreased by 25% from day 0 and diaphragmatic endurance had decreased by 36%. CONCLUSIONS: Eleven days of mechanical ventilation and neuromuscular blockade in healthy baboons resulted in nonsignificant changes in hemodynamics, oxygenation, and/or lung function. However, significant impairment in diaphragmatic endurance and strength were seen. Based on these results, it is likely that prolonged mechanical ventilation by itself impairs diaphragmatic function independent of underlying lung disease.

Animals↗
PubMed1999

Purine in bronchoalveolar lavage fluid as a marker of ventilation-induced lung injury.

OBJECTIVE: To investigate in a rat model of ventilation-induced lung injury whether metabolic changes in the lung are reflected by an increased purine concentration (adenosine, inosine, hypoxanthine, xanthine, and urate; an index of adenosine-triphosphate breakdown) of the bronchoalveolar lavage fluid and whether purine can, thus, indirectly serve as a marker of ventilation-induced lung injury. DESIGN: Prospective, randomized, controlled trial. SETTING: Research laboratory. SUBJECTS: Forty-two male Sprague-Dawley rats. INTERVENTIONS: Five groups of Sprague-Dawley rats were subjected to 6 mins of mechanical ventilation. One group was ventilated at a peak inspiratory pressure of 7 cm H2O and a positive end-expiratory pressure of 0 cm H2O. A second group was ventilated at a peak inspiratory pressure of 45 cm H2O and a positive end-expiratory pressure of 10 cm H2O. Three groups of Sprague-Dawley rats were ventilated at a peak inspiratory pressure of 45 cm H2O without positive end-expiratory pressure. Before mechanical ventilation, two of these groups received intratracheal administration of saline or exogenous surfactant at a dose of 100 mg/kg and one group received no intratracheal administration. A sixth group served as the nonventilated controls. MEASUREMENTS AND MAIN RESULTS: Bronchoalveolar lavage fluid was collected in which both purine concentration (microM; mean +/- SD) and protein concentration (mg/mL; mean +/- SD) were determined. Statistical differences were analyzed using the one-way analysis of variance (ANOVA) with a Student-Newman-Keul's post hoc test. Purine and protein concentrations were different between groups (ANOVA p value for purine and protein, <.0001). Both purine and protein concentrations in bronchoalveolar lavage fluid were increased in Group 45/0 (3.2 +/- 1.9 and 4.2 +/- 1.6, respectively) compared with Group 7/0 (0.4 +/- 0.1 [p < .05] and 0.4 +/- 0.2 [p < .001]) and controls (0.2 +/- 0.2 [p < .01] and 0.2 +/- 0.1 [p < .001]) and in Group 45/Na (5.8 +/- 2.5 and 4.2 +/- 0.5) compared with Group 7/0 (purine and protein, p < .001) and the controls (purine and protein, p < .001). Positive end-expiratory pressure prevented an increase in purine and protein concentrations in bronchoalveolar lavage fluid (0.4 +/- 0.3 and 0.4 +/- 0.2, respectively) compared with Group 45/0 (purine, p < .01; protein, p < .001) and Group 45/Na (purine and protein, p < .001). Surfactant instillation preceding lung overinflation reduced purine and protein concentration in bronchoalveolar lavage fluid (2.1 +/- 1.6 and 2.7 +/- 1.0) compared with Group 45/Na (purine, p < .001; protein (p < .01). Surfactant instillation reduced protein concentration compared with Group 45/0 (p < .01). CONCLUSIONS: This study shows that metabolic changes in the lung as a result of ventilation-induced lung injury are reflected by an increased level of purine in the bronchoalveolar lavage fluid and that purine may, thus, serve as an early marker for ventilation-induced lung injury. Moreover, the study shows that both exogenous surfactant and positive end-expiratory pressure reduce protein infiltration and that positive end-expiratory pressure decreases the purine level in bronchoalveolar lavage fluid after lung overinflation.

Analysis of Variance↗
PubMed2002

Injurious ventilation induces widespread pulmonary epithelial expression of tumor necrosis factor-alpha and interleukin-6 messenger RNA.

OBJECTIVE: We examined the hypothesis that injurious strategies of mechanical ventilation alter the expression and distribution within the lung of tumor necrosis factor-alpha and interleukin-6 that are both duration and ventilation strategy dependent. SUBJECTS: Male Sprague Dawley rats. INTERVENTIONS: Lungs from rats were preserved immediately after death or were randomized to ex vivo ventilation with either a) noninjurious ventilation; b) high end-inspiratory lung volume with positive end-expiratory pressure (PEEP); c) high end-inspiratory lung volume without PEEP; or d) intermediate lung distension without PEEP, for periods ranging from 30 mins to 3 hrs. MEASUREMENT AND MAIN RESULTS: Changes in cytokines were assessed by in situ hybridization, immunocytochemistry, simultaneous in situ hybridization and immunocytochemistry, Northern analysis, and enzyme-linked immunosorbent assay. Whereas minimal expression of tumor necrosis factor-alpha and interleukin-6 mRNA was found in lungs subjected to noninjurious ventilation, the three injurious strategies resulted in a diffuse increase in expression of tumor necrosis factor-alpha and interleukin-6. The principal cells involved were the bronchial, bronchiolar, and alveolar epithelium. The changes in tumor necrosis factor-alpha mRNA and protein expression were dependent on both duration of ventilation and the ventilation strategy used. CONCLUSIONS: The vast pulmonary epithelium is a major contributor to ventilation-induced changes in cytokine production and may play an important role in the pathogenesis of lung injury and systemic sequelae in ventilated subjects.

Animals↗
PubMed1996

Cadaver lungs for transplantation. Effect of ventilation with alveolar gas.

In an effort to increase the donor pool for lung transplantation (LTX), we have demonstrated the feasibility of LTX from circulation-arrested cadavers in a canine LTX model. We hypothesized that ventilation of the cadaver lung with alveolar gas (20% O2, 5% CO2, balance N2) (AG) would be superior to ventilation with 100% oxygen (O2) after circulatory arrest of the donor. Twelve mongrel dogs were intubated, heparinized and euthanized by pentothal injection and ventilated with AG (n=6) or O2 (n=6). Four hours later, donor animals underwent sternotomy, and the lungs were flushed with cold modified Euro-Collins solution, harvested, and stored inflated in ice slush. Left lung allotransplantation was performed, and recipients were made dependent o n the transplanted lung by occlusion of the contralateral bronchus and pulmonary artery. Recipient animals were ventilated with an FiO2 of 0.4 and followed for 8 hr. Total ischemic time was 7.9 hr for both groups. Pulmonary edema developed in all recipients of AG lungs; one recipient survived the 8-hr observation period with poor oxygenation. In contrast, three of six recipients of O2-ventilated lungs survived for 8-hr with excellent gas exchange. Specimens of donor lungs before and after transplant were evaluated histologically utilizing trypan blue exclusion as an indicator of cell viability. At the time of organ retrieval 4 hr after death, 6% of cells were nonviable in the O2-ventilated cadaver lungs. Circulation-arrested cadaver lungs ventilated with 100% O2 prior to organ retrieval have superior pulmonary function after transplant compared with lungs ventilated with AG. Ventilation of cadaver lungs with AG induces pulmonary injury in this model. retrieval of donor lungs from circulation-arrested cadavers has potential for increasing the pulmonary donor pool.

Animals↗
PubMed2004

Barriers to providing lung-protective ventilation to patients with acute lung injury.

OBJECTIVE: No studies have explored the barriers to implementing lung-protective ventilation in patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Our objective was to identify barriers to using lung-protective ventilation in patients with ALI/ARDS. DESIGN: Survey with content analysis of open-ended responses. SETTING: Medical center. PARTICIPANTS: Experienced intensive care unit nurses and respiratory therapists network identified through purposive sampling at hospitals from the ARDS Network, a National Institutes of Health-sponsored research consortium. INTERVENTIONS: Survey. RESULTS: Fifty-five surveys representing all ten ARDS Network sites were received. Twenty-seven (49%) of the respondents were intensive care unit nurses, 24 (44%) were respiratory therapists, and four did not indicate their profession. Clinicians had used lung-protective ventilation in a median of 20 (interquartile range, 10-50) patients with ALI/ARDS. Respondents identified physician willingness to relinquish control of ventilator, physician recognition of ALI/ARDS, and physician perceptions of patient contraindications to low tidal volumes as important barriers to initiating lung-protective ventilation. Important barriers to continuing patients on lung-protective ventilation were concerns over patient discomfort and tachypnea and concerns over hypercapnia, acidosis, and hypoxemia. Techniques for overcoming barriers were identified including specific ventilator setup recommendations, clinician education, and tools to assess patient discomfort. CONCLUSIONS: Experienced bedside clinicians perceive important barriers to implementing lung-protective ventilation. Successful strategies to increase use of lung-protective ventilation should target these barriers.

Attitude of Health Personnel↗
PubMed2004

Ventilation strategy affects cytokine release after mesenteric ischemia-reperfusion in rats.

OBJECTIVE: To evaluate the impact of different ventilation modalities on lung and plasma concentrations of cytokines in a model of secondary lung inflammation, mesenteric ischemia-reperfusion, in rats. DESIGN: Prospective, randomized, controlled animal study. SETTING: Research laboratory of a university. SUBJECTS: Sixty-four male adult Wistar rats weighing 320-380 g. INTERVENTIONS: Eight groups were studied. Two groups underwent no surgical procedure: They were either not ventilated or ventilated with an injurious modality consisting of 30 mL/kg tidal volume (Vt) without positive-end expiratory pressure (PEEP). Animals of the other groups underwent laparotomy with or without 2-hr mesenteric ischemia followed by 4 hrs of reperfusion during which the rats were mechanically ventilated. Ventilation modalities were conventional (tidal volume 10 mL/kg, PEEP 3 cm H2O), protective (6 mL/kg, 6 cm H(2)O), or injurious (tidal volume 30 mL/kg and no PEEP). Rats were killed by exsanguination, and their lungs were excised and homogenized in buffer. Supernatants of lung homogenates and plasmas were stored at -80 degrees C for subsequent measurements. MEASUREMENTS AND MAIN RESULTS: Tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, macrophage inhibitory protein 2, and interleukin-10 were determined in lung supernatants and plasmas with a rat-specific enzyme-linked immunosorbent assay. Lung and plasma cytokine concentrations were not significantly different between rats ventilated with the injurious modality only and nonventilated rats. Lung and plasma cytokine concentrations were higher in rats that had undergone mesenteric ischemia-reperfusion than in rats with laparotomy only, whatever ventilation modality. Lung and plasma cytokine concentrations were higher in these rats after the injurious ventilation modality than after the other modalities. CONCLUSION: This study shows that an injurious ventilation does not produce significant in vivo release of cytokines in intact animals but promotes the release of pro- and anti-inflammatory cytokines in an inflammatory context.

Animals↗
PubMed2004

Host response to intratracheally instilled bacteria in ventilated and nonventilated rats.

OBJECTIVE: Pneumonia occurs in approximately 7% of hospitalized patients. Susceptibility to certain bacteria such as Pseudomonas aeruginosa increases in critically ill patients, particularly those requiring mechanical ventilation. Previous studies investigating this susceptibility have used injurious modes of ventilation. The objective of this study was to evaluate the host's response to intratracheal instillation of P. aeruginosa in the setting of noninjurious mechanical ventilation and compare this with normal, spontaneously breathing animals receiving bacteria. DESIGN: Randomized, controlled in vivo animal study. SETTING: Research laboratory at a university-affiliated institution. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: Rats were randomized into four groups: spontaneously breathing given saline, spontaneously breathing given bacteria, mechanically ventilated given saline, and mechanically ventilated given bacteria. The ventilation strategy used involved low stretch (tidal volume of 8 mL/kg) with a positive end-expiratory pressure of 5 cm H2O. MEASUREMENTS AND MAIN RESULTS: Lung compliance, bacterial recovery, surfactant, total cells, and cytokine concentrations in the lung lavage were analyzed after 4 hrs. Results showed that neither ventilation nor bacteria alone altered lung function, although the combination of ventilation and Pseudomonas significantly decreased arterial oxygenation and lung compliance. Increases in lavage cell counts, cytokines, and surfactant were observed in both groups administered bacteria compared with animals given saline. However, there were no significant differences in bacterial recovery, cell counts, cytokines, and surfactant measurements in the groups given bacteria. CONCLUSIONS: These data suggest that bacterial instillation with low-stretch ventilation had a significant effect on lung function but did not alter the inflammatory response to a bacterial challenge over this time course compared with spontaneously breathing animals.

Animals↗
PubMed2005

Prone position delays the progression of ventilator-induced lung injury in rats: does lung strain distribution play a role?

OBJECTIVE: To investigate if prone position delays the progression of experimental ventilator-induced lung injury, possibly due to a more homogeneous distribution of strain within lung parenchyma. DESIGN: Prospective, randomized, controlled trial. SETTING: Animal laboratory of a university hospital. SUBJECTS: Thirty-five Sprague Dawley male rats (weight 257 +/- 45 g). INTERVENTIONS: Mechanical ventilation in either supine or prone position and computed tomography scan analysis. MEASUREMENTS: : Animals were ventilated in supine (n = 15) or prone (n = 15) position until a similar ventilator-induced lung injury was reached. To do so, experiments were interrupted when respiratory system elastance was 150% of baseline. Ventilator-induced lung injury was assessed as lung wet-to-dry ratio and histology. Time to reach lung injury was considered as a main outcome measure. In five additional animals, computed tomography scans (GE Light Speed QX/I, thickness 1.25 mm, interval 0.6 mm, 100 MA, 100 Kv) were randomly taken at end-expiration and end-inspiration in both positions, and quantitative analysis was performed. Data are shown as mean +/- sd. MEASUREMENTS AND MAIN RESULTS: Similar ventilator-induced lung injury was reached (respiratory system elastance, wet-to-dry ratio, and histology). The time taken to achieve the target ventilator-induced lung injury was longer with prone position (73 +/- 37 mins vs. 112 +/- 42, supine vs. prone, p = .011). Computed tomography scan analysis performed before lung injury revealed that at end-expiration, the lung was wider in prone position (p = .004) and somewhat shorter (p = .09), despite similar lung volumes (p = .455). Lung density along the vertical axis increased significantly only in supine position (p = .002). Lung strain was greater in supine as opposed to prone position (width strain, 7.8 +/- 1.8% vs. 5.6 +/- 0.9, supine vs. prone, p = .029). CONCLUSIONS: Prone position delays the progression of ventilator-induced lung injury. Computed tomography scan analysis suggests that a more homogeneous distribution of strain may be implicated in the protective role of prone position against ventilator-induced lung injury.

Animals↗
PubMed2005

Intermittent spontaneous breathing protects the rat diaphragm from mechanical ventilation effects.

OBJECTIVE: Short-term mechanical ventilation has been proven to reduce diaphragm force and fiber dimensions. We hypothesized that intermittent spontaneous breathing during the course of mechanical ventilation would minimize the effects of mechanical ventilation on diaphragm force and expression levels of transcription factors (MyoD and myogenin). DESIGN: Randomized, controlled experiment. SETTING: Animal basic science laboratory. SUBJECTS: Male Wistar rats, weighing 350-500 g. INTERVENTIONS: Anesthetized and tracheotomized rats were submitted to either 24 hrs of spontaneous breathing (SB, n = 5), 24 hrs of continuous controlled mechanical ventilation (CMV, n = 7), or controlled mechanical ventilation with intermittent spontaneous breathing: 60 mins every 5 hrs of mechanical ventilation repeated four times (ISB60, n = 8) or 5 mins every 5 hrs 55 mins of mechanical ventilation repeated four times (SB5, n = 9). They were compared with control animals free from intervention (C, n = 5). MEASUREMENTS AND MAIN RESULTS: The profile of the diaphragm force-frequency curve of the controls and SB group was significantly different from that of the ISB and CMV groups; especially, the mean asymptotic force was less in the ISB and CMV compared with controls and SB. CMV resulted in a significant decrease in the diaphragm type I (-26%, p < .05 vs. C) and type IIx/b (-39%, p < .005 vs. C and SB) cross-sectional area, whereas this was not observed in the ISB groups. Diaphragm MyoD protein expression was significantly decreased after ISB60 (-35%, p < .0001 vs. C and SB) and even more after CMV (-73%, p < .0001 vs. others). The same pattern was observed with myogenin protein levels. Positive relationships between diaphragm MyoD and myogenin protein levels and diaphragm force were observed. CONCLUSIONS: The data demonstrated that intermittent spontaneous breathing during the course of mechanical ventilation may minimize the deleterious effect of controlled mechanical ventilation on diaphragm force, fiber dimensions, and expression of transcription factors.

Animals↗
PubMed2006

Effects of tidal volume on work of breathing during lung-protective ventilation in patients with acute lung injury and acute respiratory distress syndrome.

OBJECTIVE: To assess the effects of step-changes in tidal volume on work of breathing during lung-protective ventilation in patients with acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS). DESIGN: Prospective, nonconsecutive patients with ALI/ARDS. SETTING: Adult surgical, trauma, and medical intensive care units at a major inner-city, university-affiliated hospital. PATIENTS: Ten patients with ALI/ARDS managed clinically with lung-protective ventilation. INTERVENTIONS: Five patients were ventilated at a progressively smaller tidal volume in 1 mL/kg steps between 8 and 5 mL/kg; five other patients were ventilated at a progressively larger tidal volume from 5 to 8 mL/kg. The volume mode was used with a flow rate of 75 L/min. Minute ventilation was maintained constant at each tidal volume setting. Afterward, patients were placed on continuous positive airway pressure for 1-2 mins to measure their spontaneous tidal volume. MEASUREMENTS AND MAIN RESULTS: Work of breathing and other variables were measured with a pulmonary mechanics monitor (Bicore CP-100). Work of breathing progressively increased (0.86 +/- 0.32, 1.05 +/- 0.40, 1.22 +/- 0.36, and 1.57 +/- 0.43 J/L) at a tidal volume of 8, 7, 6, and 5 mL/kg, respectively. In nine of ten patients there was a strong negative correlation between work of breathing and the ventilator-to-patient tidal volume difference (R = -.75 to -.998). CONCLUSIONS: : The ventilator-delivered tidal volume exerts an independent influence on work of breathing during lung-protective ventilation in patients with ALI/ARDS. Patient work of breathing is inversely related to the difference between the ventilator-delivered tidal volume and patient-generated tidal volume during a brief trial of unassisted breathing.

Acute Disease↗
PubMed1988

"Closing volume" during high-frequency ventilation in anesthetized dogs.

Airway closure, mean airway pressure, gas exchange and different modes of artificial ventilation were investigated in anesthetized and paralyzed dogs with clinically healthy lungs. The animals were ventilated with either intermittent positive pressure ventilation (IPPV), continuous positive pressure ventilation (GPPV, positive end-expiratory pressure (PEEP) = 0.49 kPa) or high-frequency jet ventilation (HFJV, open system) of 2 and 30 Hz with an inspiratory to expiratory (I/E) - ratio of 30/70 and 60/40. Closing volume (CV) was determined by a modified technique, submitting the lung to constant subatmospheric pressure after an inspiratory vital capacity of oxygen. Two different tests for CV were used: the foreign gas bolus (FGB) with helium as nonresident gas and the single breath nitrogen dilution technique (SBO2). During conventional mechanical ventilation, CV decreased significantly (P less than 0.05) after establishing a PEEP of 0.49 kPa. During HFJV, CV increased significantly (P less than 0.01). This effect was predominantly dependent on I/E duration time ratio and to a lesser extent on ventilatory frequency. There were significant differences between CV obtained by the FGB-method (CV(helium] and CV derived from the SBO2-test (CV(SBO2], although both tests revealed the same proportional changes of CV during the different modes of ventilation. The elevated CV was associated with a decreasing Pao2 and increasing Aa-Do2 and Paco2, indicating substantial hypoventilation and mismatching of ventilation and perfusion. Mean airway pressure increased with both CPPV and HFJV, revealing a dissociation between airway pressure and regional FRC distribution during HFJV. It is concluded that certain modes of high-frequency ventilation lead to impaired distribution of inspired gas to dependent lung regions.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗
PubMed1997

A comparison of pressure- and volume-controlled ventilation at different inspiratory to expiratory ratios.

BACKGROUND: Inverse ratio ventilation (IRV) is frequently used in severe acute respiratory failure. IRV may lead to intrinsic positive end-expiratory pressure (PEEP) and is thought to improve oxygenation and to have advantageous effects on lung mechanics. Published data to support the use of IRV are scarce. This animal study compares external PEEP with intrinsic PEEP in pressure- and volume-controlled ventilation. METHODS: Fifteen pigs were randomly treated with 1. volume-controlled PEEP ventilation (I:E ratio 1:2) (VCV PEEP), 2. volume-controlled ventilation (I:E ratio 4:1) (VCIRV) and 3. pressure-controlled ventilation (I:E ratio 4:1) (PCIRV). Baseline measurements were performed using volume-controlled ventilation (I:E ratio 1:2) (VCV ZEEP). Lung mechanics, haemodynamics and gas exchange were measured by standard methods and functional residual capacity (FRC) by the sulphur hexafluoride technique. RESULTS: In comparison to VCV PEEP, PCIRV resulted in reduced peak airway pressure (32 +/- 3 vs. 27 +/- 6 cm H2O, P < 0.001) and increased mean airway pressure (14 +/- 2 vs. 22 +/- 5 cm H2O, P < 0.001). FRC was 942 +/- 264 ml in VCV PEEP and 1024 +/- 390 ml in PCIRV (n.s.). Oxygen delivery was lower in PCIRV (458 +/- 193 vs. 346 +/- 150 ml/min, P < 0.05). Physiologic dead space was 14 +/- 4% in PCIRV and 20 +/- 6% in VCV PEEP and VCIRV (P < 0.005). CONCLUSIONS: Inverse ratio ventilation did not result in improved FRC in comparison to conventional volume-controlled PEEP ventilation. PCIRV allows for a reduction in minute ventilation but the increase in mean airway pressure compromises circulation.

Airway Resistance↗
PubMed2005

Effect of prolonged mechanical ventilation on diaphragm muscle mitochondria in piglets.

BACKGROUND: Respiratory muscle weakness is a common problem in the intensive care unit and could be involved in difficulties in weaning from the ventilator after prolonged mechanical ventilation. Animal models have shown that mechanical ventilation itself impairs diaphragm muscle function. In this study we investigated whether diaphragm contractile impairment caused by mechanical ventilation and immobilization in piglets is associated with a derangement in diaphragm mitochondria. METHODS: Seven piglets received controlled mechanical ventilation during 5 days. A control group of eight piglets were anaesthetized and surgically manipulated in the same way, but were mechanically ventilated for 4-6 h. After mechanical ventilation, diaphragm muscle biopsies were taken for measurements of mitochondria content, mitochondrial respiratory enzymes and markers of oxidative stress. RESULTS: Diaphragm mitochondrial content, as assessed by citrate synthase activities and volume density, was not different between the control and ventilated piglets. Activity of complex IV of the mitochondrial respiratory chain decreased by 21% (P=0.02) when expressed per muscle weight and by 11% (P=0.03) when expressed per citrate synthase activity. There were no changes in the markers of oxidative stress between the two groups. CONCLUSION: Five days of mechanical ventilation and immobilization decreased the activity of complex IV of the mitochondrial respiratory chain in the diaphragm muscle of the piglets.

Animals↗
PubMed2001

Patient-triggered ventilation in premature neonates.

Observed short-term benefits of patient-triggered ventilation include improvements in oxygenation and carbon dioxide elimination, reduced cerebral blood flow variability, more rapid weaning from ventilation and reduced adrenaline levels. The three multicentre randomized controlled trials in which longer term outcomes were investigated failed to demonstrate any consistent reductions in rates of pneumothorax, chronic lung disease, cranial ultrasound changes, duration of ventilation or mortality. Two of these studies were conducted wholly or predominantly using the SLE 2000 ventilator, with the Drager Babylog 8000 used in a minority of infants. The results therefore reflect only the performance of these ventilators, with the ventilation techniques used. As the degree to which synchrony was achieved was not measured in any of these studies, they provide no evidence for a lack of benefit from achieving synchronous ventilation. It is possible that the findings were influenced by the use of drugs, especially morphine and theophylline. In one study the pneumothorax rate was significantly lower in infants recruited within 3 mo of the first patient enrolled at that centre, and was seen with both modes of ventilation. This suggests that staff education in ventilation techniques may be important in reducing pneumothorax rates.

Humans↗
PubMed1993

Within-breath modulation of left ventricular function during normal breathing and positive-pressure ventilation in man.

1. To investigate how intrathoracic pressure affects left ventricular function during normal breathing and positive-pressure ventilation, beat-by-beat measurements of left ventricular stroke volume (LVSV; pulsed Doppler ultrasound), heart rate and blood pressure were made in five normal subjects breathing actively and then undergoing passive positive-pressure ventilation. 2. To assess the within-breath effects of positive-pressure ventilation on left ventricular function in the clinical setting, further measurements were made in six patients sedated, paralysed and ventilated because of brain injuries, who had no disease of the heart or lungs. 3. In the normal subjects, there were minimal phasic variation in LVSV during positive-pressure ventilation with the subject passive. Heart rate and blood pressure also stayed relatively constant throughout the ventilator cycle. During active breathing at the same depth and rate, there were large phasic respiratory variations in LVSV, with the lowest values occurring during inspiration. 4. In the paralysed and unconscious patients, an increase in LVSV was associated with the increase in airway pressure which occurred during lung inflation; however, the phase lag between the rise in airway pressure and the rise in LVSV varied widely between patients. These changes occurred whether or not sinus arrhythmia was present. 5. Addition of 4.6 +/- 1 cmH2O of positive end-expiratory pressure (PEEP) did not increase the within-breath LVSV variations, but resulted in a mean depression of LVSV of 5.4% (paired t test, P = 0.035). 6. The smaller variations in LVSV during positive-pressure ventilation compared to normal breathing in the conscious subjects may reflect (a) the smaller magnitude of positive, compared to negative, pleural pressure excursions which accompany a given tidal volume, and (b) an asymmetry between the effects of positive and negative pleural pressure on the heart. 7. The prominent effects of positive-pressure ventilation on LVSV in unconscious patients, compared to the minimal effects seen in ventilated normal subjects, may result from reduced lung compliance and a degree of pulmonary vascular congestion in the patients which was undetectable clinically or radiologically.

Adolescent↗
PubMed2006

Transporting newborn infants with suspected duct dependent congenital heart disease on low-dose prostaglandin E1 without routine mechanical ventilation.

AIM: To evaluate the safety of transporting newborn infants with suspected duct dependent congenital heart disease (CHD) treated with prostaglandin E1 (PGE1) without routine mechanical ventilation. METHODS: A retrospective population-based audit of newborn infants with suspected CHD transported on PGE1 by the New South Wales newborn and paediatric Transport Service from 1995 through 2005. RESULTS: Mechanical ventilation was not used prior to treatment with PGE1 in 94 (31%) of the 300 infants. The indications for mechanical ventilation in the remaining 206 infants (69%) included elective mechanical ventilation because of the intention to use PGE1 (n = 125) and severe hypoxaemia, acidosis or cardiorespiratory failure prior to commencing PGE1 (n = 81). 16 (17%) of the 94 infants who were not ventilated initially required mechanical ventilation before transport because of apnoea, which developed within one hour of commencing PGE1. 2 (2.6%) of the 78 infants transported without mechanical ventilation developed apnoea in transit and both were receiving >or=15 ng/kg/min of PGE1. Apnoea was more likely to occur in non-ventilated infants when the PGE1 infusion rate was >or=15 ng/kg/min compared with <15 ng/kg/min (14/33 vs 4/61, chi(2) = 15.55, p<.001). CONCLUSIONS: Newborn infants with suspected duct dependent CHD treated with low dose PGE1 (<15 ng/kg/min) may not require mechanical ventilation for safe transport.

Alprostadil↗