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

It has been postulated that sleep disruption may change ventilatory chemoresponsiveness to hypercapnia and hypoxia and thereby contribute to the development of respiratory failure in some patients with obstructive sleep apnea syndrome (OSAS) or with other respiratory disorders. Some studies have demonstrated a reduction in ventilatory chemoresponsiveness in normal subjects after one night of total sleep deprivation. However, sleep fragmentation rather than total sleep deprivation is usual in patients. In this study, therefore, we measured hypercapnic ventilatory responsiveness (HCVR) and spirometry in 13 healthy male subjects (18 to 30 yr of age) after two consecutive nights of severe sleep fragmentation (arousal to an auditory stimulus after each minute of sleep) and compared the results with those obtained in the same subjects after normal sleep. Sleep fragmentation and normal sleep were separated by a week, and the order of intervention was randomized from patient to patient. No significant differences were observed in the slope or position of the HCVR curve after sleep fragmentation or in forced expiratory volumes. Although it is possible that a more prolonged period of sleep fragmentation than that used in this study may have an effect on HCVR, the results suggest that sleep fragmentation is an unlikely cause of progressive respiratory failure in patients with OSAS or with other respiratory disorders.
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PMID:Sleep fragmentation and ventilatory responsiveness to hypercapnia. 195 42

We measured the ventilatory recruitment threshold for CO2 (RT) during wakefulness, nonrapid eye movement sleep (NREM), and rapid eye movement sleep (REM) in eight patients with respiratory failure. Because the lungs were mechanically ventilated during the RT measurements, we were able to define the effects of arousal state on the chemoresponsiveness of the unloaded respiratory system. Ventilator settings were held constant in each patient, assuring that mechanoreceptor input to the respiratory controller remained the same during all measurements. RT increased from 38 +/- 6 mm Hg during relaxed wakefulness to 42 +/- 8 mm Hg during NREM sleep (p less than or equal to 0.01), consistent with a blunting of chemoresponsiveness during sleep. In five subjects we were able to measure RT during REM sleep also. In four of them, REM RT exceeded the wakefulness measurement by at least 3 mm Hg. The remaining patient showed no demonstrable changes in RT during either sleep state. We conclude that the loss of a wakefulness stimulus contributes to sleep-induced hypercarbia in humans.
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PMID:Influence of sleep state on CO2 responsiveness. A study of the unloaded respiratory pump in humans. 195 43

Infants, children, and adolescents with chronic respiratory failure are surviving in increasing numbers and, thereby, producing a significant population of ventilator-dependent pediatric patients. Chronic respiratory failure can occur as a complication of a wide variety of disease states; in pathophysiologic terms, it generally results from either decreased central nervous system output or inadequate force generated by the respiratory pump. Its laboratory hallmark is hypercapnia with or without hypoxemia. Stabilization of the patient with mechanical ventilatory support may permit long-term survival. Management of the ventilator-dependent pediatric patient is a complex task that must begin with an accurate prognostication of each patient's survival and quality of life. Once a decision is made concerning the practicality and appropriateness of long-term ventilatory support, informed choices must be made with respect to need for an artificial airway, mode of ventilation, and location of care. Many younger patients, especially those with intrinsic lung disease (like bronchopulmonary dysplasia), may require a hospital setting for long-term care, whereas others with neuromuscular or central disorders may benefit from being discharged to home. The patient's family must be thoroughly educated in the child's care, and they must be involved in decision-making. A multidisciplinary team of physicians, therapists, nurses, and other professionals is required to deliver optimal care. Outcome is good for most patients who are carefully selected.
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PMID:The ventilator-dependent child: issues in diagnosis and management. 198 23

Extracorporeal membrane oxygenation (ECMO) has been used for 20 years in neonates and children with cardiac and respiratory failure. The number of neonates treated with ECMO has increased exponentially, but the number of older children treated is small. The selection and exclusion criteria for pediatric ECMO are poorly defined, and the results vary because of variable selection criteria and institutional experience with the technique. In order to help define the role of pediatric ECMO, we reviewed our experience in noneonatal pediatric respiratory failure. We have treated 22 patients ranging in age from 1 to 105 months and ranging in weight from 3 to 35 kg. Eighteen patients met the criteria for adult respiratory distress syndrome, two had respiratory syncytial virus pneumonia, and one had severe barotrauma complicating the management of reactive airway disease. All patients were considered by the referring institutions and by us to be failing conventional management as evidenced by hypoxia, hypercarbia, excessive ventilatory pressures, or progressive barotrauma. All were considered likely to die with continued conventional management. Sixteen of the 22 patients had complications (73%), but half of the last 10 patients had no complications. Hemorrhagic complications occurred in 12 patients. Mechanical complications included membrane failure, raceway rupture, pump malfunction, and improper cannula positioning. Other complications included culture-proven infection and renal failure. Eleven of the 22 patients survived (50%); nine of the last 12 survived (75%). These results suggest that ECMO may be a useful technique in selected pediatric patients with respiratory failure. Survival and complication rates improve as experience with the technique increases.
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PMID:Extracorporeal membrane oxygenation for nonneonatal respiratory failure. 203 Apr 80

In order to study the effect of the decrease in P-Pi caused by low pH on hemoglobin-oxygen affinity, we measured P-Pi,2,3-diphosphoglycerate (2,3-DPG), and oxygen tension at 50% saturation (P50) in 36 cases with acute exacerbation of chronic respiratory failure with hypercapnia. The cases were classified into two groups by arterial blood pH values obtained on the day of admission. Group A: pH less than or equal to 7.35 and Group B: pH greater than or equal to 7.36. P50 was calculated by a modification of Severinghaus' equation developed by Yusa and Kohsaka, and it was corrected by applying the carboxy-hemoglobin (COHb) coefficient. On the day of admission (stage I), 2,3-DPG and P50 in both groups were slightly higher than in the control group. In Group A, a week after admission (stage II), these values decreased and became significantly lower than they had been at stage I. Especially 2,3-DPG in stage II was even lower than those of the control group. Approximately 14 days after admission, in stage III, it was found that these values had risen to the initial level at stage I. In Group A, similar changes were also observed for P-Pi. The value of P-Pi was low in stage II and recovered to the initial value in stage III. On the other hand, we found that the urinary excretion of phosphorus (U-Pi) increased at stage I in Group A. It was supposed that the increase in U-Pi at stage I caused a decrease in P-Pi, which caused the decrease in 2,3-DPG, in stage II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemoglobin-oxygen affinity in acute exacerbation of chronic respiratory failure]. 207

The percentage of the patients with PaCO2 more than 60 Torr and PaO2 more than 50 Torr were 13% in the patients with tuberculosis sequela (N = 502) and 4% in the patients with chronic obstructive lung disease (COLD, N = 727), who were treated with home oxygen therapy in the western region of Japan. Patients with chronic respiratory failure caused by tuberculosis sequela have higher PaCO2 than patients with COLD. Although the prognosis of patients with hypercapnia and moderate hypoxemia is not necessarily poor, some patients may need treatment for severe hypoventilation to prevent respiratory muscle fatigue and abnormal breathing during sleep. In this study, nine patients with hypercapnic chronic respiratory failure caused by tuberculosis sequela were ventilated by Chest Negative Pressure Ventilation (CNPV). The patients were monitored as in polysomnography by transcutaneous PCO2 (PtcCO2) electrode and Respiratory Inductance Plethysmography (RIP). Tidal volume induced by CNPV was larger during mouth breathing (504 +/- 128 ml, mean +/- s.d.) than during nose breathing (438 +/- 109 ml) calculated from RIP in awake state (N = 7). Oxygen saturation measured by ear oximeter and PtcCO2 were 94.4 +/- 2.9% and 57.8 +/- 12.2 Torr in awake state. Following CNPV SaO2 and PtcCO2 were 95.7 +/- 3.0%, 42.7 +/- 12.1 Torr in awake state (N = 9) and 93.0 +/- 4.4%, 57.0 +/- 15.7 Torr in Non-REM sleep (N = 5), respectively. CNPV is effective in these patients in awake state. During Non-REM sleep, CNPV maintains the PtcCO2 level only in awake state.
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PMID:[Tuberculosis sequelae: pathophysiological aspect (ventilation)]. 207 61

The value of mechanical ventilation using intermittent positive pressure ventilation delivered non-invasively by nasal mask was assessed in six patients with life threatening exacerbations of chronic respiratory disease. Median (range) arterial oxygen and carbon dioxide tensions were 4.4 (3.5-7.2) kPa and 8.7 (5.5-10.9) kPa respectively, with four patients breathing air and two controlled concentrations of oxygen. The arterial oxygen tension increased with mechanical ventilation to a median (range) of 8.7 (8.0-12.6) kPa and the carbon dioxide tension fell to 8.2 (6.5-9.2) kPa. Four patients discharged after a median of 10 (8-17) days in hospital were well five to 22 months later. One died at four days of worsening sputum retention and another after five weeks using the ventilator for 12-16 hours each day while awaiting heart-lung transplantation. This technique of mechanical ventilation avoids endotracheal intubation and can be used intermittently. Hypercapnic respiratory failure can be relieved in patients with either restrictive or obstructive lung disease in whom controlled oxygen treatment results in unacceptable hypercapnia. Respiratory assistance can be tailored to individual need and undertaken without conventional intensive care facilities.
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PMID:Non-invasive mechanical ventilation for acute respiratory failure. 233 29

The long term outcome for 88 patients with bullous emphysema who had operations was analysed from the clinical, respiratory function and occupational point of view. In order to reduce to the minimum any bias which would be likely to appear as a result of a decrease in the number of patients with time respiratory function parameters were compared to those of a restricted number of patients for whom we knew all the values for each period determined. Before the operation all the patients showed radiological signs of bullous emphysema; the respiratory function measurements in 66 of them showed bronchial obstruction with distension, hypoxaemia at rest without hypercapnia. The clinical follow up and respiratory function was spread over more years. It showed a post operative improvement in dyspnoea which was perceptible in 77% of patients at 2 years, 68% at 3 years, 60% at 4 years, 51% at 5 years, 32% at 10 years. 2/3 of the patients who were working before the operation had taken up their normal work following it. the survival levels were 86% at 1 year, 83% at 2 years, 80% at 3 years, 78% at 4 years, 77% at 5 years, 73% at 6 years, 73% at 6 years, 58% at 10 years. Of 20 patients who died 12 had died of respiratory failure. All the spirographic parameters had improved following the operation but a secondary deterioration was noted around the 5th post operative year for the vital capacity, and at the third year for residual volume, FEV 1, and the FEV 1/VC ratio as well as PAO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term outcome of surgically treated bullous emphysema]. 210 80

Animal studies have demonstrated that mechanical ventilation with high peak inspiratory pressure (PIP) results in acute lung injury characterised by hyaline membranes, granulocyte infiltration and increased pulmonary and systemic vascular permeability. This can result in progressive respiratory failure and death. In surfactant deficient lungs this occurs with tidal volumes (Vt) as low as 12 ml/kg, and PIP as low as 25 cm H2O, values which are frequently used clinically. The mechanisms resulting in this form of ventilator induced lung injury are not clear, but it appears to result from global or regional overdistension of the lung or terminal airways. It can be prevented or reduced in severity in some animal models by the use of PEEP. It is suggested that the use of high PIP in some patients may result in progressive deterioration of their ARDS, possibly contributing to mortality both from respiratory failure and other causes. It may be very important to limit PIP by reducing Vt even if this results in hypercapnia and a deterioration of oxygenation in the short term.
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PMID:Ventilatory management of ARDS: can it affect the outcome? 219 41

Respiratory failure accompanied by cardiac failure occurs mostly due to decreased PaO2. However, sometimes we encounter patients with cardiac failure having on increase of PaCO2, who develop CO2 narcosis in the ICU. In this study we evaluated hypoventilation respiratory failure in patients with cardiac failure. Seventy-six patients with both respiratory failure and cardiac failure caused by intrinsic heart disease, who required mechanical ventilation in the ICU were studied. The patients were divided into 2 groups; hypoxic respiratory failure group (n = 53) and hypoventilation respiratory failure group (n = 23). Blood gas analysis and cardiovascular hemodynamics including arterial blood pressure, heart rate and Swan-Ganz catheter findings were performed before, during and after mechanical ventilation in each patient. Mortality rate and its relation to hemodynamic variables were also evaluated in each group. In both groups even when it was possible to maintain oxygenation capacity by conducting mechanical ventilation against severe respiratory failure, what can be said about the prognosis is that it depended totally on the improvement of cardiac function. The mechanism by which hypoxemia is displayed due to cardiogenic pulmonary edema is already well known, but in regard to the mechanism of hypercapnia in cases with hypersensitivity of the airways it is thought that through induction of cardiogenic pulmonary edema bronchial spasms is induced, and this causes hypercapnia. However, it is also possible to consider cardiac asthma as the cause. Among respiratory failure cases due to cardiogenic pulmonary edema that occurs in association with heart failure, there is both hypoxic respiratory failure as well as hypoventilation respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study on the respiratory failure with cardiac failure--focus on hypoventilation respiratory failure]. 221 87


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