8 resultados para Respiratory Dead Space
em BORIS: Bern Open Repository and Information System - Berna - Suiça
Resumo:
Sleep disordered breathing with central apnea or hypopnea frequently occurs at high altitude and is thought to be caused by a decrease in blood CO(2) level. The aim of this study was to assess the effects of added respiratory dead space on sleep disordered breathing.
Resumo:
BACKGROUND: The time course of impairment of respiratory mechanics and gas exchange in the acute respiratory distress syndrome (ARDS) remains poorly defined. We assessed the changes in respiratory mechanics and gas exchange during ARDS. We hypothesized that due to the changes in respiratory mechanics over time, ventilatory strategies based on rigid volume or pressure limits might fail to prevent overdistension throughout the disease process. METHODS: Seventeen severe ARDS patients {PaO2/FiO2 10.1 (9.2-14.3) kPa; 76 (69-107) mmHg [median (25th-75th percentiles)] and bilateral infiltrates} were studied during the acute, intermediate, and late stages of ARDS (at 1-3, 4-6 and 7 days after diagnosis). Severity of lung injury, gas exchange, and hemodynamics were assessed. Pressure-volume (PV) curves of the respiratory system were obtained, and upper and lower inflection points (UIP, LIP) and recruitment were estimated. RESULTS: (1) UIP decreased from early to established (intermediate and late) ARDS [30 (28-30) cmH2O, 27 (25-30) cmH2O and 25 (23-28) cmH2O (P=0.014)]; (2) oxygenation improved in survivors and in patients with non-pulmonary etiology in late ARDS, whereas all patients developed hypercapnia from early to established ARDS; and (3) dead-space ventilation and pulmonary shunt were larger in patients with pulmonary etiology during late ARDS. CONCLUSION: We found a decrease in UIP from acute to established ARDS. If applied to our data, the inspiratory pressure limit advocated by the ARDSnet (30 cmH2O) would produce ventilation over the UIP, with a consequent increased risk of overdistension in 12%, 43% and 65% of our patients during the acute, intermediate and late phases of ARDS, respectively. Lung protective strategies based on fixed tidal volume or pressure limits may thus not fully avoid the risk of lung overdistension throughout ARDS.
Resumo:
Velopharyngeal insufficiency in cleft patients with muscular insufficiency detected by nasendoscopy is commonly treated by secondary radical intravelar veloplasty, in which the palatal muscles are reoriented and positioned backwards. The dead space between the retro-displaced musculature and the posterior borders of the palatal bone remains problematic. Postoperatively, the surgically achieved lengthening of the soft palate often diminishes due to scar tissue formation in the dead space, leading to reattachment of the reoriented muscles to the palatal bone and to decreased mobility of the soft palate. To avoid this, the dead space should be restored by a structure imitating the function of the missing palatal aponeurosis. The entire dead space was covered using a double layer of autogenous fascia lata harvested from the lateral thigh, which should allow sufficient and permanent sliding of the retro-positioned musculature. A clinical case of a 9-year-old boy who underwent the operation is reported. Postoperatively, marked functional improvements were observable in speech assessment, nasendoscopy and nasometry. The case reported here suggests that the restoration of the dead space may be beneficial for effective secondary palatal repair. Fascia lata seems to be a suitable graft for this purpose.
Resumo:
Soft tissue coverage of the medial ankle and foot remains a difficult, challenging, and often frustrating problem to patients as well as surgeons. To our knowledge, the abductor hallucis muscle flap is not frequently used and only a few well documented cases were found in literature. The purpose of this paper is to report and to present the long-term results of a series of four patients who underwent reconstruction of foot and ankle defects with the abductor hallucis muscle flap.In two cases, the abductor hallucis muscle flap was transposed in combination with a medialis pedis flap to cover a medial ankle defect, whereas in another case it was combined with a medial plantar flap. In this latter case, the muscle flap served to fill up a calcaneal dead space after osteomyelitis debridement, whereas the cutaneous flap was used to replace debrided skin at the heel. The abductor hallucis flap was used as a distally-based turnover flap to cover a large forefoot defect in a fourth case. Follow-up period ranged between 18 and 64 months (mean 43.3). In the early postoperative period, two flaps healed completely In two patients marginal flap necrosis occurred which was subsequently skin grafted. No donor-site complication occurred in any of the patients. In all cases, protective sensation of the skin was satisfactory as early as 6 months. In two cases mild hyperkeratosis at the skin graft border to the sole skin (non-weight bearing area of medial plantar and medialis pedis flap donor site) was present, but probably related to poor foot care. All patients were fully mobile as early as 3 months after treatment. In the long-term follow-up (43.3 months), all flaps provided with durable coverage. Functional gait deficit due to consumtion of the abductor hallucis muscle was not apparent.Our long-term results demonstrated that the abductor hallucis muscle flap is a versatile, and reliable flap suitable for the reconstruction of foot and ankle defects. Utilizing the abductor hallucis muscle as a pedicled flap (distally or proximally-based) with or without conjoined regional fasciocutaneous flaps offers a successful and durable alternative to microsurgical tree flaps for small to moderate defects over the calcaneus region, medial ankle, medial foot, and forefoot with exposed bone, tendon, or joint.
Resumo:
The aim of this study was to test the effect of cardiac output (CO) and pulmonary artery hypertension (PHT) on volumetric capnography (VCap) derived-variables. Nine pigs were mechanically ventilated using fixed ventilatory settings. Two steps of PHT were induced by IV infusion of a thromboxane analogue: PHT25 [mean pulmonary arterial pressure (MPAP) of 25 mmHg] and PHT40 (MPAP of 40 mmHg). CO was increased by 50 % from baseline (COup) with an infusion of dobutamine ≥5 μg kg(-1) min(-1) and decreased by 40 % from baseline (COdown) infusing sodium nitroglycerine ≥30 μg kg(-1) min(-1) plus esmolol 500 μg kg(-1) min(-1). Another state of PHT and COdown was induced by severe hypoxemia (FiO2 0.07). Invasive hemodynamic data and VCap were recorded and compared before and after each step using a mixed random effects model. Compared to baseline, the normalized slope of phase III (SnIII) increased by 32 % in PHT25 and by 22 % in PHT40. SnIII decreased non-significantly by 4 % with COdown. A combination of PHT and COdown associated with severe hypoxemia increased SnIII by 28 % compared to baseline. The elimination of CO2 per breath decreased by 7 % in PHT40 and by 12 % in COdown but increased only slightly with COup. Dead space variables did not change significantly along the protocol. At constant ventilation and body metabolism, pulmonary artery hypertension and decreases in CO had the biggest effects on the SnIII of the volumetric capnogram and on the elimination of CO2.
Resumo:
BACKGROUND AND OBJECTIVES Multiple-breath washout (MBW) is an attractive test to assess ventilation inhomogeneity, a marker of peripheral lung disease. Standardization of MBW is hampered as little data exists on possible measurement bias. We aimed to identify potential sources of measurement bias based on MBW software settings. METHODS We used unprocessed data from nitrogen (N2) MBW (Exhalyzer D, Eco Medics AG) applied in 30 children aged 5-18 years: 10 with CF, 10 formerly preterm, and 10 healthy controls. This setup calculates the tracer gas N2 mainly from measured O2 and CO2concentrations. The following software settings for MBW signal processing were changed by at least 5 units or >10% in both directions or completely switched off: (i) environmental conditions, (ii) apparatus dead space, (iii) O2 and CO2 signal correction, and (iv) signal alignment (delay time). Primary outcome was the change in lung clearance index (LCI) compared to LCI calculated with the settings as recommended. A change in LCI exceeding 10% was considered relevant. RESULTS Changes in both environmental and dead space settings resulted in uniform but modest LCI changes and exceeded >10% in only two measurements. Changes in signal alignment and O2 signal correction had the most relevant impact on LCI. Decrease of O2 delay time by 40 ms (7%) lead to a mean LCI increase of 12%, with >10% LCI change in 60% of the children. Increase of O2 delay time by 40 ms resulted in mean LCI decrease of 9% with LCI changing >10% in 43% of the children. CONCLUSIONS Accurate LCI results depend crucially on signal processing settings in MBW software. Especially correct signal delay times are possible sources of incorrect LCI measurements. Algorithms of signal processing and signal alignment should thus be optimized to avoid susceptibility of MBW measurements to this significant measurement bias.
Resumo:
OBJECTIVE: To describe clinical respiratory parameters in cats and dogs with respiratory distress and identify associations between respiratory signs at presentation and localization of the disease with particular evaluation between the synchrony of abdominal and chest wall movements as a clinical indicators for pleural space disease. Design - Prospective observational clinical study. SETTING: Emergency service in a university veterinary teaching hospital. ANIMALS: Cats and dogs with respiratory distress presented to the emergency service between April 2008 and July 2009. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The following parameters were systematically determined at time of admission: respiratory rate, heart rate, temperature, type of breathing, movement of the thoracic and abdominal wall during inspiration, presence of stridor, presence and type of dyspnea, and results of thoracic auscultation. Abdominal and chest wall movement was categorized as synchronous, asynchronous, or inverse. Diagnostic test results, diagnosis, and outcome were subsequently recorded. Based on the final diagnoses, animals were assigned to 1 or more of the following groups regarding the anatomical localization of the respiratory distress: upper airways, lower airways, lung parenchyma, pleural space, thoracic wall, nonrespiratory causes, and normal animals. One hundred and seventy-six animals (103 cats and 73 dogs) were evaluated. Inspiratory dyspnea was associated with upper airway disease in dogs and expiratory dyspnea with lower airway disease in cats. Respiratory noises were significantly associated and highly sensitive and specific for upper airway disease. An asynchronous or inverse breathing pattern and decreased lung auscultation results were significantly associated with pleural space disease in both dogs and cats (P<0.001). The combination is highly sensitive (99%) but not very specific (45%). Fast and shallow breathing was not associated with pleural space disease. Increased or moist pulmonary auscultation findings were associated with parenchymal lung disease. CONCLUSIONS: Cats and dogs with pleural space disease can be identified by an asynchronous or inverse breathing pattern in combination with decreased lung sounds on auscultation.
Resumo:
A morphological and morphometric study of the lung of the newborn quokka wallaby (Setonix brachyurus) was undertaken to assess its morphofunctional status at birth. Additionally, skin structure and morphometry were investigated to assess the possibility of cutaneous gas exchange. The lung was at canalicular stage and comprised a few conducting airways and a parenchyma of thick-walled tubules lined by stretches of cuboidal pneumocytes alternating with squamous epithelium, with occasional portions of thin blood-gas barrier. The tubules were separated by abundant intertubular mesenchyme, aggregations of developing capillaries and mesenchymal cells. Conversion of the cuboidal pneumocytes to type I cells occurred through cell broadening and lamellar body extrusion. Superfluous cuboidal cells were lost through apoptosis and subsequent clearance by alveolar macrophages. The establishment of the thin blood-gas barrier was established through apposition of the incipient capillaries to the formative thin squamous epithelium. The absolute volume of the lung was 0.02 +/- 0.001 cm(3) with an air space surface area of 4.85 +/- 0.43 cm(2). Differentiated type I pneumocytes covered 78% of the tubular surface, the rest 22% going to long stretches of type II cells, their precursors or low cuboidal transitory cells with sparse lamellar bodies. The body weight-related diffusion capacity was 2.52 +/- 0.56 mL O(2) min(-1) kg(-1). The epidermis was poorly developed, and measured 29.97 +/- 4.88 microm in thickness, 13% of which was taken by a thin layer of stratum corneum, measuring 4.87 +/- 0.98 microm thick. Superficial capillaries were closely associated with the epidermis, showing the possibility that the skin also participated in some gaseous exchange. Qualitatively, the neonate quokka lung had the basic constituents for gas exchange but was quantitatively inadequate, implying the significance of percutaneous gas exchange.