A respiratory drive in addition to the increase in CO(2) production at raised body temperature in rats.
(17/494)
Mammals that use the ventilatory system as the principal means of increasing heat loss, i.e. that pant, show two fundamental changes in the control of breathing at raised temperatures. First, alveolar ventilation increases by more than, rather than in proportion to, the increase in CO2 production. Second, hypocapnia no longer causes apnoea. Rats do not use the ventilatory system as the principal means of increasing heat loss, so we have investigated whether rats also show these two changes at raised temperatures. Breathing was detected from diaphragmatic electromyogram (EMG) activity. Anaesthesia and hyperoxia were used to minimise behavioural and hypoxic drives to ventilation and arterial PCO2 (Pa,CO2) was controlled using mechanical ventilation. At 36.6 +/- 0.1 >C, breathing was absent as long as Pa,CO2 was held below a threshold level of 32.9 +/- 0.7 mm Hg (n = 14) under steady-state conditions. When body temperature in rats was raised above 37 >C, both fundamental changes in the control of breathing became apparent. First, at 39 >C the mean Pa,CO2 level during spontaneous breathing (39.6 +/- 5.4 mm Hg, n = 4) fell by 3.9 +/- 1.4 mm Hg (P < 0.05, Student's paired t test). Second, at 39.9 +/- 0.1 >C breathing was present when mean Pa,CO2 levels were only 18.2 +/- 1.5 mm Hg (n = 14), the lowest mean Pa,CO2 level we could achieve with mechanical ventilation. We calculate, however, that at 39.9 >C, the drive to breathe from the increased CO2 production alone would not sustain breathing below a Pa,CO2 level of 27.8 +/- 1.4 mm Hg (n = 13). In rats at raised body temperatures therefore a respiratory drive exists that is in addition to that related to the increase in CO2 production. (+info)
Laboratory assessment of the Bird T-Bird VS ventilator performance using a model lung.
(18/494)
We assessed the Bird T-Bird VS ventilator using a model lung constructed to standard 10651-1 of the International Standards Organization. We used different combinations of lung compliance and airway resistance to simulate normal and diseased adult and paediatric lungs. Different preset tidal volumes at various respiratory rates were delivered to the model lung and compared with the actual measured tidal volumes. The results showed that the delivered tidal volumes were within the manufacturer's specification of +/- 10% of the preset tidal volumes in normal adult and paediatric combinations of lung compliance and airway resistance. The ventilator can be powered by mains electricity supply or battery and requires only optional compressed oxygen. The ventilator is suitable for the provision of advanced ventilatory support during prolonged patient transfer. (+info)
A new ventilator for monitoring lung mechanics in small animals.
(19/494)
Researchers investigating the genetic component of various disease states rely increasingly on murine models. We have developed a ventilator to simplify respiratory research in small animals down to murine size. The new ventilator provides constant-flow inflation and tidal volume delivery independent of respiratory parameter changes. The inclusion of end-inspiratory and end-expiratory pauses simplifies the measurement of airway resistance and compliance and allows the detection of dynamic hyperinflation (auto-positive end-expiratory pressure). After bench testing, we performed intravenous methacholine challenge on two strains of mice (A/J and C57bl/bj) known to differ in their responses by using the new ventilator. Dynamic hyperinflation and a decrease in compliance developed during methacholine challenge whenever respiratory rates of 60-120 breaths/min were employed. In contrast, if dynamic hyperinflation was prevented by lengthening expiratory time, (respiratory rate = 20 breaths/min), static compliance remained constant. More importantly, the coefficient of variation of the results decreased when lung volume shifts were prevented. In conclusion, airway challenge studies have greater precision when dynamic hyperinflation is prevented. (+info)
Invited review: mechanisms of ventilator-induced lung injury: a perspective.
(20/494)
Despite advances in critical care, the mortality rate in patients with acute lung injury remains high. Furthermore, most patients who die do so from multisystem organ failure. It has been postulated that ventilator-induced lung injury plays a key role in determining the negative clinical outcome of patients exposed to mechanical ventilation. How mechanical ventilation exerts its detrimental effect is as of yet unknown, but it appears that overdistension of lung units or shear forces generated during repetitive opening and closing of atelectatic lung units exacerbates, or even initiates, significant lung injury and inflammation. The term "biotrauma" has recently been elaborated to describe the process by which stress produced by mechanical ventilation leads to the upregulation of an inflammatory response. For mechanical ventilation to exert its deleterious effect, cells are required to sense mechanical forces and activate intracellular signaling pathways able to communicate the information to its interior. This information must then be integrated in the nucleus, and an appropriate response must be generated to implement and/or modulate its response and that of neighboring cells. In this review, we present a perspective on ventilator-induced lung injury with a focus on mechanisms and clinical implications. We highlight some of the most recent findings, which we believe contribute to the generation and propagation of ventilator-induced lung injury, placing a special emphasis on their implication for future research and clinical therapies. (+info)
In vitro compound A formation in a computer-controlled closed-circuit anesthetic apparatus. Comparison with a classical valve circuit.
(21/494)
BACKGROUND: Few data exist on compound A during sevoflurane anesthesia when using closed-circuit conditions and sodalime with modern computer-controlled liquid injection. METHODS: A PhysioFlex apparatus (Drager, Lubeck, Germany) was connected to an artificial test lung (inflow approximately 160 ml/min carbon dioxide, outflow approximately 200 ml/min, simulating oxygen consumption). Ventilation was set to obtain an end-tidal carbon dioxide partial pressure (Petco2) approximately 40 mmHg. Canister inflow (T degrees in) and outflow (T degrees out) temperatures were measured. Fresh sodalime and charcoal were used. After baseline analysis, sevoflurane concentration was set at 2.1% end-tidal for 120 min. At baseline and at regular intervals thereafter, Petco2, end-tidal sevoflurane, T degrees in, and T degrees out were measured. For inspiratory and expiratory compound A determination, samples of 2-ml gas were taken. These data were compared with those of a classical valve-containing closed-circuit machine. Ten runs were performed in each set-up. RESULTS: Inspired compound A concentrations increased from undetectable to peak at 6.0 (SD 1.3) and 14.3 (SD 2.5) ppm (P < 0.05), and maximal temperature in the upper outflow part of the absorbent canister was 24.3 degrees C (SD 3.6) and 39.8 degrees C (SD 1.2) (P < 0.05) in the PhysioFlex and valve circuit machines, respectively. Differences between the two machines in compound A concentrations and absorbent canister temperature at the inflow and outflow regions were significantly different (P < 0.05) at all times after 5 min. CONCLUSION: Compound A concentrations in the high-flow (70 l/min), closed-circuit PhysioFlex machine were significantly lower than in conventional, valve-based machines during closed-circuit conditions. Lower absorbent temperatures, resulting from the high flow, appear to account for the lower compound A formation. (+info)
The preoptic area in the hypothalamus is the source of the additional respiratory drive at raised body temperature in anaesthetised rats.
(22/494)
In mammals that use the ventilatory system as the principal means of increasing heat loss, raising body temperature causes the adoption of a specialised breathing pattern known as panting and this is mediated by the thermoregulatory system in the preoptic area of the hypothalamus. In these species an additional respiratory drive is also present at raised body temperature, since breathing can reappear at low Pa,CO2 levels, when stimulation of chemoreceptors is minimal. It is not known whether the preoptic area is also the source of this additional drive. Rats do not pant but do possess this additional respiratory drive at raised body temperatures. We have therefore tested whether the preoptic area of the hypothalamus is the source of this additional respiratory drive in rats. Urethane anaesthesia and hyperoxia were used in eleven rats to minimise behavioural and chemical drives to breathe. The presence of the additional respiratory drive was indicated if rhythmic diaphragmatic EMG activity reappeared during hypocapnia (a mean Pa,CO2 level of 21+/-2 mm Hg, n = 11), induced by mechanical ventilation. The additional respiratory drive was absent at normal body temperature (37 inverted question markC). When the temperature of the whole body was raised using an external source of radiant heat, the additional respiratory drive appeared at 40.6+/-0.5 degrees C (n = 3). In two further rats this drive was induced at normal body temperature by localised warming in the preoptic area of the intact hypothalamus. The additional respiratory drive appeared at similar temperatures to those in control rats in three rats following isolation of the hypothalamus from more rostral areas of the brain. In contrast, the additional respiratory drive failed to appear at these temperatures in three rats after isolating the hypothalamus from the caudal brainstem, by sectioning pathways medial to the medial forebrain bundle. Since the preoptic area is known to contain thermoreceptors and to receive afferents from peripheral thermoreceptors, the results show that this area is also the source of the additional respiratory drive at raised body temperature in anaesthetised rats. (+info)
Pressure-time curve predicts minimally injurious ventilatory strategy in an isolated rat lung model.
(23/494)
BACKGROUND: We tested the hypothesis that the pressure-time (P-t) curve during constant flow ventilation can be used to set a noninjurious ventilatory strategy. METHODS: In an isolated, nonperfused, lavaged model of acute lung injury, tidal volume and positive end-expiratory pressure were set to obtain: (1) a straight P-t curve (constant compliance, minimal stress); (2) a downward concavity in the P-t curve (increasing compliance, low volume stress); and (3) an upward concavity in the P-t curve (decreasing compliance, high volume stress). The P-t curve was fitted to: P = a. tb +c, where b describes the shape of the curve, b = 1 describes a straight P-t curve, b < 1 describes a downward concavity, and b > 1 describes an upward concavity. After 3 h, lungs were analyzed for histologic evidence of pulmonary damage and lavage concentration of inflammatory mediators. Ventilator-induced lung injury occurred when injury score and cytokine concentrations in the ventilated lungs were higher than those in 10 isolated lavaged rats kept statically inflated for 3 h with an airway pressure of 4 cm H2O. RESULTS: The threshold value for coefficient b that discriminated best between lungs with and without histologic and inflammatory evidence of ventilator-induced lung injury (receiver-operating characteristic curve) ranged between 0.90-1.10. For such threshold values, the sensitivity of coefficient b to identify noninjurious ventilatory strategy was 1.00. A significant relation (P < 0.001) between values of coefficient b and injury score, interleukin-6, and macrophage inflammatory protein-2 was found. CONCLUSIONS: The predictive power of coefficient b to predict noninjurious ventilatory strategy in a model of acute lung injury is high. (+info)
Surgical stabilization of traumatic flail chest.
(24/494)
Since 1970 we have stabilized the ribs to correct paradoxical movement of the chest wall in chest injuries, using an original technique, in order to avoid as far as possible the need for long-term chest wall stabilization by intermittent positive pressure respiration (IPPR). The technical details of surgical stabilization are described, and the different types of stainless steel struts are shown. Type I was originally used either as an intramedullary nail or as an external brace. Types II and III were designed for external fixation of the strut to the rib. Treatment of 29 patients with severe flail chest, classified into four groups is shown: group I was treated by IPPR, group II by IPPR plus surgical stabilization, group III by surgical stabilization only, and group IV by surgical stabilization after exploratory thoracotomy. The clinical results are discussed. We conclude that surgical stabilization of the paradoxial movement of the chest wall can avoid the use of the respirator or at least reduce the interval of IPPR to a short period during the initial recovery from trauma. Using type III struts, we have obtained stabilization of the flail chest in all cases even in patients with severe anterior paradoxical movement. The patients' tolerance of surgical stainless steel struts was good. (+info)