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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A progressive pulmonary disease resulting in severe respiratory failure and death in an average of 3 weeks was diagnosed in 11 young Dalmatian dogs. The dogs were from 4 litters, all genetically related by a common ancestor. The initial clinical signs were tachypnea and noisy respiration. Respiratory distress developed shortly before death and was characterized by strenuous and rapid respirations, along with cyanosis and vomiting. On blood gas analysis, there were severe arterial hypoxemia, hypercapnia, and marked alveolar-arterial oxygen difference. Radiographically, a diffuse pattern of alveolar, interstitial, and peribronchial densities was observed in the lungs. Most dogs developed pneumomediastinum and gastroesophageal intussusception in the terminal phase of the disease. There was no response to treatment with antibiotics, corticosteroids, diuretics, or oxygen. At necropsy, the lungs were wet, heavy, and relatively airless. Absence of 1 kidney in 2 dogs and severe internal hydrocephalus in 2 dogs were additional necropsy findings. Pulmonary histopathology included metaplasia and atypia of the alveolar and bronchiolar epithelium, a nonpurulent inflammatory reaction characterized mainly by mononuclear cells and macrophages, eosinophilic hyaline membrane formation, and focal pulmonary fibrosis. The histological manifestations were typical of acute lung injury. Clinically, the findings were consistent with adult respiratory distress syndrome (ARDS), except for the relatively long course. No known risk factors for ARDS, such as trauma, toxin exposure, infection, or endotoxemia could be identified. The relationship of the other abnormalities (ie, renal aplasia, hydrocephalus) to the pulmonary disease also remains obscure. An inherited defect is suspected, because segregation analysis of the 4 litters suggests autosomal recessive inheritance.
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PMID:Lung injury leading to respiratory distress syndrome in young Dalmatian dogs. 767 17

The catastrophic pulmonary failure that complicates management of patients with multiple trauma or sepsis syndrome with shock is recognizable to nearly all experienced surgeons. However, the spectrum of injury is broad, the distribution of lung injury may be heterogeneous within a single patient, and many patients will not develop acute respiratory distress syndrome (ARDS) even after a major predisposing insult. The lung responds stereotypically to many disparate insults, so a better conceptual construct of ARDS may be to consider it as one component of the multiple organ dysfunction syndrome. Support of oxygen transport with positive pressure ventilation and high levels of positive end-expiratory pressure, long the mainstay of pulmonary support, has been criticized for its predilection to cause barotrauma. Newer modes of ventilation, such as pressure-controlled, inverse-ratio ventilation and permissive hypercapnia, are under investigation but have not yet been reported with scientific rigor. However, pulmonary support extends beyond the support of gas exchange. Fluid management requires close attention so that the circulation is supported but lung water accumulation is minimized. Nosocomial pneumonia greatly increases the mortality rate in ARDS, but is difficult to diagnose and must be sought aggressively. Until recently, pharmacologic therapy has held little promise, but inhalation of very low concentrations of nitric oxide appear to decrease pulmonary vascular pressures and intrapulmonary shunt. It remains unknown whether nitric oxide is effective therapy for the underlying injury, or is simply treatment for certain manifestations.
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PMID:Organ-specific support in multiple organ failure: pulmonary support. 767 4

Recent studies and reviews continue to report a high mortality associated with the acute respiratory distress syndrome (ARDS), which involves a severe inflammatory reaction within the whole lung that is frequently associated with multiple-organ failure. Important factors contributing to the poor results in severe ARDS are the aggressive procedures required to maintain sufficient arterial oxygenation, such as mechanical ventilation with high inspiratory pressures and high inspired oxygen concentrations (FiO2) which themselves contribute to the progression of the disease. As no specific therapy that reduces or prevents the general inflammatory reaction is known, current therapy is limited to procedures that minimize peak inspiratory pressures and FiO2. Therefore, pressure- and volume-limited ventilation modes with positive end-expiratory pressure, controlled hypercapnia, differential lung ventilation when appropriate, positioning (particularly prone), and aggressive dehydration are used. Should these procedures fail to improve arterial gas exchange, the patients may be additionally treated by veno-venous extracorporeal gas exchange. To reduce the risk of severe haemorrhagic complications due to high levels of systemic heparinization, systems internally coated with covalently bound heparin, which allow a lower level of systemic anticoagulation, should be used. From April 1989 to August 1993, 89 patients were transferred to our intensive care unit for treatment of severe ARDS; 52 were treated by combining the described conventional methods without artificial gas exchange (survival rate 88%) and 37 additionally underwent artificial gas exchange (survival rate 57%). The overall survival rate was 75%. On the basis of these experiences, we conclude that this step-by-step approach may improve survival in patients with severe ARDS.
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PMID:[Therapy of ARDS. 1. Current therapeutic strategy including extracorporeal gas exchange]. 804 58

A key element of neonatal regionalization is the establishment of transport links between centres of tertiary care and subregional centres. During the 11-year period 1982-92, 186 transports were undertaken from the neonatal unit, Vestfold Central Hospital, for a total of 180 patients, or 0.8% of all live born infants (n = 23,652). 64 patients (36%) were referred for prematurity/respiratory distress syndrome (IRDS), 81 (45%) for congenital malformations, and 35 (19%) for other conditions. Transports for prematurity/IRDS declined significantly from the the first 6-year period 1982-87 to the last 5-year period 1988-92 (3.6 vs. 1.8 per 1,000 live born infants; p < 0.01), owing to the establishment of a local respirator treatment programme for severe IRDS. In 71 (38%) transports the infants were mechanically ventilated. Seven (10%) suffered in-transport complications related to the endotracheal tube. At arrival, significantly more patients were anaemic (Hb < 14 g%; transports before 48 hours after birth), alcalotic (pH > 7.50), hypocapnic (PCO2 < 4 kPa) or had a base excess < -10 mmol/l than before transportation (p < 0.05). There was a tendency towards more patients with hypothermia (tp < 36 degrees C), acidosis (pH (< 7.20) and hypercapnia (PCO2 > 10 kPa) at arrival than before transportation (p > 0.05). No deaths occurred during transport. However, two infants died within two hours after arrival, giving a transport-related mortality rate of 1%. Transporting critically ill neonates implies discontinuity of treatment and monitoring of these infants. Optimal stabilization before transportation, and scrupulous work on technical details are of utmost importance.
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PMID:[Transport from a subregional neonatal unit. Experiences from Vestfold Central Hospital during an 11-year period 1982-92]. 825 80

Alveolar overdistention and cyclic reopening of collapsed alveoli have been implicated in the lung damage found in animals submitted to artificial ventilation. To test whether these phenomena are impairing the recovery of patients with acute respiratory distress syndrome (ARDS) submitted to conventional mechanical ventilation (MV), we evaluated the impact of a new ventilatory strategy directed at minimizing "cyclic parenchymal stretch." After receiving pre-established levels of hemodynamic, infectious, and general care, 28 patients with early ARDS were randomly assigned to receive either MV based on a new approach (NA, consisting of maintenance of end-expiratory pressures above the lower inflection point of the P x V curve, VT < 6 ml/kg, peak pressures < 40 cm H2O, permissive hypercapnia, and stepwise utilization of pressure-limited modes) or a conventional approach (C = conventional volume-cycled ventilation, VT = 12 ml/kg, minimum PEEP guided by FIO2 and hemodynamics and normal PaCO2 levels). Fifteen patients were selected to receive NA, exhibiting a better evolution of the PaO2/FIO2 ratio (p < 0.0001) and of compliance (p = 0.0018), requiring shorter periods under FIO2 > 50% (p = 0.001) and a lower FIO2 at the day of death (p = 0.0002). After correcting for baseline imbalances in APACHE II, we observed a higher weaning rate in NA (p = 0.014) but not a significantly improved survival (overall mortality: 5/15 in NA versus 7/13 in C, p = 0.45). We concluded that the NA ventilatory strategy can markedly improve the lung function in patients with ARDS, increasing the chances of early weaning and lung recovery during mechanical ventilation.
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PMID:Beneficial effects of the "open lung approach" with low distending pressures in acute respiratory distress syndrome. A prospective randomized study on mechanical ventilation. 852 Jul 44

1. The possible contribution of endogenous endothelin (ET) to the pathogenesis of seizure-associated pulmonary oedema was examined in mechanically ventilated rats after intravenous bolus injection of the gamma-aminobutyric acid (GABA) antagonist, bicuculline (1.2 mg kg-1). 2. Recurrent seizure activity elicited by bicuculline injection led to rapidly developing pulmonary oedema. Within 4 min after bicuculline application (1.2 mg kg-1), arterial O2 partial pressure (PaO2) significantly dropped from 17.49 +/- 1.20 kPa to 7.51 +/- 2.21 kPa (P < 0.01) and arterial CO2 partial pressure (PaCO2) significantly increased from 4.64 +/- 0.56 kPa to 8.15 +/- 0.99 kPa (P < 0.01). Gradually a progressive acidosis developed. Moreover, mean arterial blood pressure (MABP) and end-inspiratory airway pressure (Paw) rapidly increased. 3. Concomitantly there was a time-dependent increase of big ET-1 and ET-1 levels in bronchoalveolar lavage (BAL) as determined by combined reverse phase high performance liquid chromatography (h.p.l.c.) and radioimmunoassay. BAL levels of both peptides increased up to 8 min after bicuculline injection and slowly decreased subsequently. In contrast, BAL from animals injected with vehicle did not contain detectable amounts of ET. 4. Pretreatment with the endothelin-converting enzyme inhibitor, phosphoramidon (5.4 mg kg-1, i.v.) for 5 min significantly (P < 0.001) reduced peak ET-1 levels in BAL fluid by 65.4 +/- 9.9% at 8 min after bicuculline injection. Simultaneously it afforded protection from hypoxia. PaCO2 did not increase and PaO2 decreased only slightly from 14.63 +/- 1.00 kPa to 12.97 +/- 0.61 kPa (P > 0.05) after phosphoramidon pretreatment. In contrast, vehicle-treated animals that received bicuculline showed both significant hypercapnia as well as profound hypoxia. Phosphoramidon significantly diminished the maximum increase in Paw by 76.7 +/- 12.4% (P <0.005), but only slightly affected the MABP. Phosphoramidon pretreatment had no effect on the acidosis.5. Pretreatment with the ETA receptor antagonist, BQ-123 (1 mg kg-1, i.v.), for 5 min did not affect the levels of ET-1 in the BAL fluid at 8 min after bicuculline injection but did ameliorate the development of hypoxia. No hypercapnia developed and Pa02 decreased only moderately from 16.65 +/-0.25 kPa to 14.19 +/-2.15 kPa (P>0.05) in BQ-123-treated animals. In contrast, vehicle-treated animals that received bicuculline exhibited significant hypercapnia as well as profound hypoxia. BQ-123 significantly reduced the increase in Paw by 51.3 +/- 12.8% (P < 0.01). It affected MABP only slightly and had no effect on the acidosis.6. These results suggest that ET peptides play a significant role in this model of neurogenic pulmonary oedema and may act as mediators of respiratory distress. The deleterious effects of endogenous ET in this model are primarily mediated via the ETA receptor, for they were inhibited by the ETA receptor antagonist, BQ-123. ETA receptor antagonists may therefore be of potential therapeutic value in respiratory distress.
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PMID:A role for endothelin in bicuculline-induced neurogenic pulmonary oedema in rats. 854 73

The mortality of patients with acute respiratory distress syndrome (ARDS) is still above 50% despite continuous progress in intensive care medicine. Recent therapy regimens such as the extra corporeal life support (ECLS), permissive hypercarbia, high-frequency ventilation techniques and inhaled nitric oxide (NO) are being applied. All of the above techniques are aimed at different parts of the problems caused by ARDS. This study was designed to evaluate the possible additive benefits of superimposed high-frequency jet ventilation (SHFJV) and inhaled NO. METHODS. In experiments on a lung simulator it was demonstrated that it is possible to administer exact amounts of NO using a computer-controlled system with a feedback loop (Pulmonox) using the SHFJV. Applying the therapeutic reference point of 20 ppm of NO, the deviation was +/- 3 ppm at this setting. CASE REPORT. After successfully concluding our experiments, this combined therapy concept was applied in a patient with terminal ARDS. Under CMV, paO2 was 69.4 mm Hg and the oxygen saturation 88.3% with a F1O2 of 1.0. Significant improvement was observed within 30 min after starting SHFJV with inhaled NO (paO2 282.9 mm Hg; oxygen saturation 99.5%). There were no differences observed in hemodynamic parameters between CMV and SHFJV. Although the pulmonary status of the patient improved, the patient died due to therapy-resistant hemodynamic failure. CONCLUSION. It will take further studies to judge whether the success of this new ventilation strategy is reproducible and if the improvement of the oxygenation is more pronounced when adding inhaled NO to SHFJV than when each technique is applied separately.
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PMID:[Superimposed high-frequency jet ventilation (SHFJV) in the administration of NO. Technical basis and early clinical results with ARDS]. 859 58

Continuous intra-arterial blood gas monitoring is a new technique, possibly offering therapeutic advantages through improved monitoring in patients prone to hypoxaemia, hypercapnia and/or respiratory acidosis. Therefore, we studied the clinical applicability, reliability, precision and side effect of long-term continuous intra-arterial blood gas monitoring in patients suffering from severe acute respiratory distress syndrome. In 10 patients continuous intra-arterial blood gas monitoring based on fluorescent optodes technique was performed. At 4 h intervals, arterial blood samples for in vitro blood gas analyses were drawn, stored in ice, and analysed within 3 min. Evaluation of data retrieved from the continuous intra-arterial blood gas monitoring and in vitro blood gas analysis was based on 596 data points using 10 catheters. Average length of insertion was 281 +/- 215 h, max. lengths of stay was 750 h. Arterial blood gas data obtained in vivo were compared to the mean of in vivo and in vitro arterial blood gases. Inter-catheter bias, expressed as percent difference between continuous intra-arterial blood gas and mean in vitro blood gas analysis was 0.19 +/- 0.23% for pH. 1.1 +/- 5.2% for PaCO2 and 1.6 +/- 5.7% for PaO2. No significant gas partial pressure dependent change in precision was demonstrable. There was no significant time dependent drift in sensor precision over the study period. No negative side-effects related to IABG monitoring were observed. We conclude that long-term use of this new device is possible in patients and represents a reliable alternative to conventional in vitro arterial blood gas analysis, when continuous monitoring of blood gases and/or acid-base balance is critical.
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PMID:Preliminary evaluation of a new continuous intra-arterial blood gas monitoring device. 859 2

Mortality of severe acute respiratory distress syndrome (ARDS) in Germany is about 60%. Respiratory therapy can make the lung injury worse by high positive airway pressures, high tidal volumes and high inspiratory oxygen concentrations. Extracorporeal membrane oxygenation (ECMO) was employed to reduce aggressive mechanical ventilation, but it has not been proved to be superior to conventional ventilation. However, encouraged by recently developed improvements in the technique and concept of ECMO, we introduced this therapy into our program for the treatment of ARDS. PATIENTS AND METHODS. All patients with severe ARDS (lung injury score > 2.5) admitted to our multidisciplinary intensive care unit from March 1992 to March 1995 were evaluated prospectively. After admission, the patients first underwent a conventional therapeutic approach, including pressure-controlled inverse-ratio ventilation, permissive hypercapnia, changes in body position (in particular, the prone position), negative fluid balance, anti-biotics, and low-dose hydrocortisone infusion. ECMO via a covalently heparin-coated, venovenous bypass-system with a vortex pump and two membrane lungs was performed if ARDS did not improve after 24-96 h of conventional therapy and if two of three of the slow-entry criteria for ECMO were fulfilled: (1) PaO2/FiO2 < 150 mmHg at PEEP > 5 mbar; (2) semistatic compliance < 30 ml/mbar; (3) right-left shunt > 30%. Only in cases of life-threatening hypoxemia (PaO2 < 50 mmHg at FiO2 1.0 and PEEP > 5 mbar for > 2 h (fast-entry criteria) was ECMO instituted immediately. RESULTS. Sixty patients fulfilled the entry criteria for our study. Thirty-nine patients were treated with a conventional protocol, 37 after improvement of ARDS and 2 who had not improved but in whom there were contraindications to the use of ECMO. ECMO was performed in 10 patients who had not improved, but who fulfilled the slow-entry criteria and in 11 primarily hypoxemic patients who fulfilled the fast-entry criteria. The survival rate was 30/39 (77%) for the conventional therapy group, 6/10 (60%) for the slow-entry group, and 11/11 (100%) for the fast-entry group. The onset of ECMO allowed a significant decrease in peak and mean airway pressures, tidal volume, ventilatory rate, minute volume and inspiratory oxygen concentration. Sufficient gas exchange was provided, and pulmonary artery pressures significantly decreased on bypass. The most frequent complications on bypass were pneumothorax (15/21 patients) and bleeding (7/21 patients). CONCLUSION. In comparison with the historical results at our own institution, the present study demonstrates an improvement in the survival rate from 56% to 78% since ECMO has become available. We conclude that venovenous ECMO with a heparin-bonded bypass circuit is an effective additional option for the treatment of patients with severe ARDS.
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PMID:[Venovenous extracorporeal membrane oxygenation (ECMO) with a heparin-lock bypass system. An effective addition in the treatment of acute respiratory failure (ARDS)]. 877 3

The relationship between total bilirubin binding capacity (TBBC) and clinical status was investigated in order to assess the risk of bilirubin toxicity in 83 infants with jaundice in this study. Infants with respiratory distress, acidosis, hypoglycaemia, sepsis, asphyxia-anoxia and hypercarbia were accepted as ill and the remainders were well. Sephadex G-25 gel filtration method was used to determine TBBC. Serum albumin levels, TBBC and TBBC/albumin molar ratios were lower in ill premature and mature infants. Acidosis was the major risk factor for bilirubin toxicity in ill infants. Therefore, clinical status should be taken into consideration in the management of jaundiced infants.
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PMID:The influence of clinical status on total bilirubin binding capacity in newborn infants. 882 Jun 20


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