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

Current recommendations for mechanical ventilation in the acute respiratory distress syndrome (ARDS) include the use of small tidal volumes (VT), even at the cost of respiratory acidosis. We evaluated the effects of this permissive hypercapnia on pulmonary gas exchange with the multiple inert gas elimination technique (MIGET) in eight patients with ARDS. After making baseline measurements, we induced permissive hypercapnia by reducing VT from 10 +/- 2 ml/kg to 6 +/- 1 ml/kg (mean +/- SEM) at constant positive end-expiratory pressure. After restoration of initial VT, we infused dobutamine to increase cardiac output (Q) by the same amount as with hypercapnia. Permissive hypercapnia increased Q by an average of 1.4 L. min(-)(1). m(2), decreased arterial oxygen tension from 109 +/- 10 mm Hg to 92 +/- 11 mm Hg (p < 0.05), markedly increased true shunt (Q S/Q T), from 32 +/- 6% to 48 +/- 5% (p < 0.0001), and had no effect on the dispersion of VA/Q.VA/Q. On reinstatement of baseline V T with maintenance of a high Q, Q S/Q T remained increased, to 38 +/- 6% (p < 0.05), and Pa(O(2 ))remained decreased, to 93 +/- 4 mm Hg (p < 0. 05). These results agreed with effects of changes in VT and Q predicted by the mathematical lung model of the MIGET. We conclude that permissive hypercapnia increases pulmonary shunt, and that deterioration in gas exchange is explained by the combined effects of increased Q and decreased alveolar ventilation.
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PMID:Permissive hypercapnia impairs pulmonary gas exchange in the acute respiratory distress syndrome. 1090 43

In patients with acute respiratory distress syndrome (ARDS), permissive hypercapnia is a strategy to decrease airway pressures to prevent ventilator-induced lung damage by lowering tidal volumes and tolerating higher arterial carbon dioxide tension. However, in experimental studies hypercapnia impairs myocardial contractility and hemodynamic function. We investigated the effect of short-term permissive hypercapnia on myocardial contractility and hemodynamics in patients with ARDS. We hypothesized that the administration of tromethamine (THAM), a buffer which does not increase carbon dioxide production, would modify these changes. In 12 patients with ARDS, permissive hypercapnia was implemented for 2 h with a target Pa(CO(2))of 80 mm Hg. Patients were randomized to have respiratory acidosis corrected by THAM (pH-corrected group), or not corrected (pH-uncorrected group). Hemodynamic responses were measured, and transesophageal echocardiography (TEE) was used to determine myocardial contractility. Permissive hypercapnia resulted in significant decreases in systemic vascular resistance (SVR) and increases in cardiac output (Q). Myocardial contractility decreased in both groups but significantly less in the pH-corrected group (approximately 10%) than in the pH-uncorrected group (approximately 18%, p < 0.05). Mean arterial pressure decreased and mean pulmonary arterial pressure increased significantly only in the pH-uncorrected group. All values returned to baseline conditions 1 h after permissive hypercapnia was terminated. Our study demonstrates a reversible depression of myocardial contractility and hemodynamic alterations during rapid permissive hypercapnia which were attenuated by buffering with THAM. This may have applicability to the clinical strategy of permissive hypercapnia and allow the benefit of decreased airway pressures to be realized while minimizing the adverse hemodynamic effects of hypercapnic acidosis.
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PMID:Tromethamine buffer modifies the depressant effect of permissive hypercapnia on myocardial contractility in patients with acute respiratory distress syndrome. 1102 45

Meconium Aspiration Syndrome (MAS) is a leading cause of respiratory distress in the newborn. Antenatal diagnosis of meconium stained amniotic fluid and fetal distress is important to reduce morbidity and mortality in the neonates. Amnioinfusion of saline and tracheal suctioning of meconium are preventive interventions. Babies with MAS who continue to have respiratory distress need to be put on conventional ventilators. Increasing hypoxia, hypercarbia and barotrauma warrants changing to high frequency oscillatory ventilation. Pulmonary hypertension is an important complication which should be promptly recognized. Nitric oxide therapy used with high frequency ventilation has improved the outcome of babies with severe MAS and pulmonary hypertension. Some of these babies who continue to worsen clinically need to be put on ECMO circuit. Surfactant infusion in babies with MAS has been shown to improve gas exchange, resolve pulmonary hypertension and decrease oxygenation index. Total and partial liquid ventilation with perflurocarbon improves oxygenation, increases lung expansion and increases pulmonary blood flow in model studies of animals with MAS. Surfactant infusion and liquid ventilation are newer promising modes of therapeutic interventions in babies with severe MAS.
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PMID:Advances in management of meconium aspiration syndrome. 1121 85

In infants with esophageal atresia (EA), lung opacities on a chest radiograph (CXR) are usually considered the cause of respiratory distress (RD). However, in some instances signs of RD and CXR changes show no correlation. The aim of this study was to investigate the pathogenesis of RD in EA patients with a normal CXR. In 41 infants with EA, CXR findings were correlated with clinical manifestations and blood-gas analysis data. The degree of abnormal gas exchange was quantitated by the arterial/alveolar oxygen tension ratio (a-ARO2). Of the 41 infants, 39(95%) presented with RD. No lung opacities were found in 130 of 294 CXRs examined (44%). An a-ARO2 below 0.75 (lower limit of normal) was calculated in 215 of 247 arterial blood samples analyzed (87%). When a temporal correlation was established, RD with a clear CXR was characterized by signs of extra- and intrathoracic airway obstruction, often associated with an a-ARO2 below 0.75. The degree of hypoxemia was greater than the degree of hypercapnia. We conclude that in infants with EA, RD with a clear CXR is related to both tracheomalacia and upper-airway obstruction that may cause miliary atelectasis not detected by conventional CXR with intrapulmonary shunting and hypoxemia.
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PMID:Respiratory status of infants with esophageal atresia. 1131 11

Acute Respiratory Failure (ARF) results in an inability to maintain gas exchange at a rate commensurate with the demands of the body and results in hypoxemia and/or hypercarbia, the mechanisms of which may be different. Hypoxemia commonly occurs due to Ventilation Perfusion (V/Q) mismatching, intrapulmonary shunt, diffusion defect or hypoventilation. Hypercarpnic respiratory failure may also be multifactorial but is usually due to inhibited central respiratory drive or inefficient respiratory muscle pump. Hypercapnia may occur in upper and lower airways obstruction, respiratory muscle fatigue and occasionally due to excess CO2 production (burns and excessive glucose administration). Issues in management centre around assessment of severity, determining the need for intervention, establishing diagnosis and etiology and institution of specific treatment. Diagnosis of respiratory failure may be made clinically and confirmed by blood gas analysis. Calculation of oxygenation indices will delineate extent of hypoxemia. When evaluating a child with respiratory failure, one should be aware that a child with prominent respiratory symptoms may have non-respiratory disease (i.e. metabolic acidosis, DKA) and conversely, advanced respiratory failure may be present in a child with no respiratory distress (central hypoventilation secondary to drugs, infection) careful assessment of history, complete physical examination and evaluation of lab parameters may clarify the diagnosis. Serial assessment of sensorium, respiratory symptoms, ABG and response to treatment will provide valuable clues to determine the need for intervention. Oxygen, like any drug, must be administered in a prescribed dose, only when indicated with the potential risks borne in mind. A variety of oxygen delivery devices are available; which ever device is used, the resulting FiO2 and devisable end points must be clearly determined. Hazards of oxygen therapy range from retinal damage in premature infants, damage to the alveolar capillary membrane with resultant hypoxemia) atelectasis and decreased mucociliary activity.
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PMID:Acute respiratory failure and oxygen therapy. 1133 23

The ARDS (acute respiratory distress syndrome) Network study found 22% lower mortality in acute lung injury and ARDS patients ventilated with low tidal volumes (V(T)) than in those ventilated with traditional V(T) ventilation. Several points should be considered when using the low V(T) protocol for clinical practice. Prior to implementation, hemodynamic and acid-base status, minute ventilation, and adequacy of sedation should be assessed to minimize the potential for intolerance. The volume-preset, assist-control mode is recommended for better control of V(T), and the respiratory rate should be increased as V(T) is reduced, so as to maintain minute ventilation and prevent acute hypercapnia. When unavoidable, hypercapnia should be induced slowly. Ventilator inspiratory flow (V(I)) and trigger sensitivity settings should be optimized to limit the increase in work of breathing and dyspnea. When dyspnea results in double-triggered breaths, V(T) can be titrated to 7-8 mL/kg, provided end-inspiratory plateau pressure is < or = 30 cm H(2)O. In severe acidosis (pH < 7.15) V(T) also can be increased. However, every effort should be made to maintain plateau pressure and V(T) goals by buffering severe acidosis and treating patient-ventilator asynchrony with sedation. Evaluation for weaning should occur when adequate oxygenation can be maintained on 40% oxygen and a positive end-expiratory pressure of 8 cm H(2)O. Pressure support levels between 5 and 20 cm H(2)O (above 5 cm H(2)O positive end-expiratory pressure) are used for weaning and titrated to keep the respiratory rate < 35 breaths/min. Pressure support levels should be weaned aggressively, as long as the protocol's weaning tolerance criteria can be maintained.
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PMID:Implementation of a low tidal volume ventilation protocol for patients with acute lung injury or acute respiratory distress syndrome. 1157 55

A 24-week premature infant developed severe right-sided pulmonary barotrauma secondary to mechanical ventilation for respiratory distress syndrome (RDS). High-frequency oscillatory ventilation and permissive hypercapnia were initiated. A chest tube was placed to relieve a pneumothorax, and a catheter was inserted into an air-filled cyst for drainage. These maneuvers failed to improve the child's respiratory status. The child's left main-stem bronchus was then successfully fiberoptically intubated for single-lung ventilation in order to reduce the unilateral barotrauma. Single-lung ventilation was effectively and safely continued for 5 days, with complete resolution of the pulmonary barotrauma.
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PMID:Selective fiberoptic left main-stem intubation for severe unilateral barotrauma in a 24-week premature infant. 1183 4

Management of congenital diaphragmatic hernia has changed dramatically over the past couple of decades. Until the early 1980s, it was felt that the abdominal contents should be returned to the abdomen as soon as possible to allow the lungs to expand. It is now known that it is not the defect that causes respiratory distress, but the infant's hypoplastic lungs and accompanying pulmonary hypertension. Advances in treatment and technology have contributed to changes in management. Ultrasonography now allows for early prenatal detection. Prenatal treatment modalities include in utero tracheal ligation and maternal antenatal steroids. Postnatal modalities have expanded to include permissive hypercapnia, high-frequency ventilation, inhaled nitric oxide, pharmacologic support, exogenous surfactant, and extracorporeal membrane oxygenation. Liquid ventilation and lobar lung transplantation have also been tried. In spite of these advances, the overall survival rate remains about 63 percent.
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PMID:Current and emerging treatment for congenital diaphragmatic hernia. 1214 12

The use of low tidal volumes with permissive hypercapnia in patients with acute respiratory distress syndrome may require heavy sedation to allow them to tolerate mechanical ventilation. Administration of methadone for sedation is an alternative to using other opioids, given its longer elimination half-life and incomplete cross-tolerance with other mu-receptor-active opioids. Methadone appears to have a molecular structure similar to that of verapamil, a calcium channel blocker, and may exhibit similar cardiac properties as well. A 43-year-old man with acute respiratory distress syndrome experienced bradycardia while receiving a continuous infusion of methadone for sedation and mechanical ventilation management. This case report demonstrates that caution is warranted when high dosages of methadone are administered because of its potential cardiac effects.
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PMID:Bradycardia associated with intravenous methadone administered for sedation in a patient with acute respiratory distress syndrome. 1222 59

There are limited data on the volumes used to ventilate infants with respiratory distress syndrome (RDS). There are no data on the volumes to aim for to avoid hypocapnia or unacceptable levels of hypercapnia. In this pilot study we measured minute volumes (MV) in ventilated infants to determine whether MV can predict arterial carbon dioxide (PaCO(2)) within acceptable parameters. Low birth weight infants (n = 14) mechanically ventilated for RDS had lung function recorded (n = 53) as an arterial blood gas was taken. MVs were plotted against PaCO(2) giving the regression equation for prediction of PaCO(2) (mm Hg) with MV (ml/kg/min): PaCO(2) = 58.3 - 0.075 x MV, r = 0.62, r(2) = 0.38, p < 0.001, residual variance (s(2)) of 52.7 (s = 7.26). 95% CI give a predicted PaCO(2) +/- 15 mm Hg for a given MV. A MV of 200 ml/kg/min predicts a PaCO(2) of 43 mm Hg (95% Cl 29-58). PaCO(2) correlates reasonably well with MV. Setting appropriate MVs may allow closer targeting of PaCO(2), and prevent over- or under-ventilation.
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PMID:Determining the ventilatory volumes required to ventilate low birth weight infants with respiratory distress syndrome. Prediction of arterial carbon dioxide using minute volumes. 1238 30


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