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

Of 100 consecutive patients with severe head injury who arrived at a major trauma center, half of whom came direct from the accident site and half from another hospital, potentially serious systemic insults to the brain were present in 44 cases. Arterial hypotension (13 cases), anemia (12 cases), and hypercarbia (4 cases) were almost exclusively associated with multiple injuries, which were present in 57 patients and were caused usually by vehicular accidents. Hypoxia was seen in 30 patients, including several with brain injury alone. These systemic insults to the already injured brain were associated with an increase in mortality and morbidity. We believe that direct transfer to a trauma center that has full-time neurosurgical facilities for victims of automobile accidents and patients who have been rendered unconscious by a fall or blow on the head will increase survival. Care for the patient with head injuries should start at the roadside.
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PMID:Early insults to the injured brain. 66 Aug 88

2,3-DPG and P50 were measured in 23 patients with chronic obstructive lung disease. All patients had a chronic hypercapnia (PaCO2 greater than or equal to 45 Torr). They are shared in 3 groups, according to hemoglobin content [Hb] and hypoxia : group I(PaO2 = 48.0 +/- 2.4 Torr ; [Hb] = 15.9 +/- 0.3 g. 100 ml-1; n = 9), (M +/- 1 SE); group II (PaO2 = 46.4 +/- 5.0 Torr; [Hb] = 11.6 +/- 0.7 g. 100 m[-1; n = 7); group III(PaO2 = 61.4 +/- 2.4 Torr; [Hb] = 13.3 +/- 0.4 g. 100 ml-1; n = 7). 2,3-DPG (group I : 1.05 +/- 0.06 mole.moleHb-1; group II : 1.02 +/- 0.08; group III : 1.11 +/- 0.08) was not significantly different of 2,3-DPG value of 12 control subjects (0.96 +/- 0.04). P50 of group I (26.9 +/- 0.9 Torr) and group III patients (28.1 +/- 1.6 Torr) was not significantly different of control value of P50 (27.4 +/- 0.5 Torr). P50 of group II patients (29.6 +/- 0.8 Torr) was significantly higher than P50 control and group I values (p less than 0.05). All the patients of group II died. These results suggest that in patients with chronic obstructive lung disease : 1) P50 value is different with various clinical conditions; 2) P50 increase is a compensatory mechanism in severe hypoxemia with anemia, but is not sufficient; 3) [Hb] is the best data for clinical prognosis.
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PMID:[Study of P50 and 2,3-diphosphoglycerate in 23 bronchoemphysema patients as a function of hypoxia and hemoglobin concentration]. 89 17

Six black infants and young children with high titers of milk precipitins were identified by screening the sera of 160 children with idiopathic chronic lung disease. None of the six had immunoglobulin deficiency, elevation of sweat chlorides, SS hemoglobin, or recurrent aspiration. All six children had typical manifestations of milk-induced pulmonary hemosiderosis: recurrent pulmonary infiltrates (6/6), hemosiderin-laden pulmonary macrophages (5/6), intermittent wheezing (5/6), eosinophilia (4/6), anemia (4/6), iron deficiency (4/4), failure to thrive (4/6), and elevated levels of serum IgE (4/4). Three children also had chronic rhinitis and eventually developed large adenoids, hypercapnia and acidosis during sleep, and right heart failure. Elimination of cow milk from the diet, symptomatic therapy, and adenoidectomy when indicated resulted in improvement of all six patients. Pulmonary hemosiderosis and some cases of upper airway obstruction with pulmonary hypertension appear to be two stages, early and delayed, of the same immunophysiologic process. Early dietary intervention may prevent the cardiovascular complications of this process.
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PMID:Hyperreactivity to cow milk in young children with pulmonary hemosiderosis and cor pulmonale secondary to nasopharyngeal obstruction. 117 19

Various techniques for support and control of respiration in neonatal foals are described. It is crucial to evaluate respiration through frequent arterial blood gas analysis. Details for blood sampling from the metatarsal arteries and interpretation of results are provided. Typical diseases in newborn foals, which cause hypoxemia and/or hypercapnia and can be indications for respiratory support are apnea, hypopnea, pulmonary atelectasis, surfactant deficiency, meconium-, fetal fluid- and milk aspiration, maladjustment syndrome, cardiovascular abnormalities, anemia, airway obstruction, compromised lung expansion, increased abdominal pressure and pneumonias. Oxygen insufflation can be delivered through an intranasal tube. Positive pressure ventilation is best accomplished via an endotracheal tube. A nasogastric tube is inserted for enteral nutrition, application of drugs and checking for gastric reflux. Details for insertion of endotracheal and nasogastric tubes are given. Positive pressure ventilation can be achieved by manual ventilation with a rebreathing resp. resuscitator bag and mechanical ventilation with a respirator. Management and control of mechanical ventilation as well as intensive care and monitoring of foals are described.
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PMID:[Respiratory support techniques in foals in a newborn intensive care unit for large animals]. 144 May 96

Artifacts or mechanical problems may cause data which suggest poor myocardial performance during emergence from cardiopulmonary bypass (CPB). Transducer and monitoring equipment malfunctions, damping of the arterial blood pressure tracing, effects of drugs, hypercarbia, inordinately high intrathoracic pressure, cardiac tamponade, and others are all possible culprits. It is important to have a systematic plan for evaluating and interpreting the signs and data that are evident. Causes of hypotension after CPB include low hematocrit, hypercarbia, sympathetic inhibition, vasodilator action, anaphylaxis or anaphylactoid reactions, protamine reactions, and impaired myocardial performance. Impaired myocardial performance can be attributable to rate and rhythm disturbances, inadequate ventricular preload, inappropriately elevated right and left ventricular afterload, and decreased myocardial contractility. Common causes of hypoxemia include a malfunctioning ventilator system, pulmonary problems such as atelectasis and shunt, anemia, and inordinately high utilization of oxygen.
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PMID:The anesthesiologist's response to a low-output state after cardiopulmonary bypass: etiologies and remedies. 213 54

Some parameters of oxygen transport blood function have been studied prior to hemodialysis treatment and following 5, 25, 50 and 100 hemodialysis procedures. It has been established that programmed hemodialysis decreases O2 transport and reserve. These changes may be associated with an unfavourable effect of the procedure itself on the body, accompanied by anemia, microthromboembolisms in lung vessels, hypercapnia and arteriovenous blood shunt. Partial compensation of O2 transport decrease is achieved due to cardiac output increase and O2 tissue excretion. These compensatory mechanisms cannot ensure normal values of O2 reserve and transport and are fairly quickly depleted in the course of hemodialysis.
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PMID:[Changes in the oxygen transport function in patients with chronic kidney failure during hemodialysis]. 271 74

This study identifies a subgroup of critically ill patients most likely to develop at least creatine kinase-myocardial isoenzyme (CK-MB) evidence of acute myocardial injury. This group is composed of patients with shock syndromes associated with some combination of anemia, hypoxemia, hypercarbia, acidemia, lactic acidosis, and hypotension. The mechanism of this secondary myocardial injury in shock is not clear but may be multifactorial. Certainly subgroups of patients admitted with critical illnesses may have CK-MB abnormalities usually associated with acute myocardial injury.
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PMID:Secondary myocardial injuries. 650 98

1. Changes in ventilation volume (Vg) of rainbow trout caused by hypercapnia, hypoxia and anaemia were measured directly by collection of expired water. 2. Exposure to hypercapnic water (PCO2 range 0.5-2 kPa) increased Vg (by up to four times) by augmenting ventilatory stroke volume; breathing frequency remained constant. O2 added to the inspired water in maintained hypercapnia reduced Vg at all but the highest level of PCO2. 3. Vg increased when blood oxygen content was decreased by exposure to normoxic hypercapnia, but addition of O2 to the water increased blood oxygen content and Vg decreased. 4. When blood oxygen-carrying capacity was depressed by hypoxia or anaemia, Vg increased as it did during normoxic hypercapnia. 5. We suggest that ventilatory responses to low levels of hypercapnia, to hyperoxic hypercapnia, to hypoxia, and to anaemia in trout are related to changes in levels of blood oxygen content under these conditions.
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PMID:The effect of changes in blood oxygen-carrying capacity on ventilation volume in the rainbow trout (Salmo gairdneri). 680 26

Effect of increased blood O2 affinity on cardiac output and its distribution was studied in conscious sedated rats by the microsphere-reference sample method. After a preliminary measurement of cardiac output and its distribution, rats were exchange transfused with normal blood or low-P50 (PO2 at which hemoglobin is half-saturated with O2) blood; other groups were made anemic with and without a simultaneous reduction in P50. Reduction in P50 from 38 to 17 Torr did not change cardiac output, pulse, or blood pressure but caused, after allowance for changes in controls, a 102% increase in coronary blood flow and an 88% increase in cerebral blood flow. Anemia (hematocrit = 22%) produced similar changes in coronary and cerebral flow. When anemia was combined with a 12-Torr reduction in P50, coronary and cerebral flow increased by 297 and 209%, respectively. These increases in coronary and cerebral flow were not attributable to increased cardiac work or hypercapnia. It is concluded that a left shift of the O2 dissociation curve induces increased blood flow to brain and heart, probably in compensation for decreased tissue O2 pressure.
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PMID:Effect of increased oxygen affinity and anemia on cardiac output and its distribution. 717 22

The prevention and treatment of secondary insults to the brain of systemic origin in severely head injured patients remain of utmost importance. Head injury remains the leading cause of traumatic death, being responsible for 50-60% of fatalities. Head-injured patients not only suffer from the primary injury at the time of trauma, but also from the secondary, largely ischaemic, brain damage that occurs later. Some of these insults are of extracranial origin (or systemic), such as arterial hypotension, hypoxaemia, hypercarbia and anaemia. Their impact on mortality and morbidity is extremely high and requires greater efforts in improving the care of head-injured patients. Systemic insults occur either before the patient reaches hospital or during interfacility transfer or, in a surprisingly large number of cases, within hospital during emergency procedures, intrahospital transport or during their stay in intensive care units. Hypoxaemia, although quite easy to treat, is still common. This calls for better and earlier protection of the airway, more systematic administration of oxygen to trauma patients and wider use of pulse oximetry. Arterial hypotension has even more dramatic consequences in severe head injury. Recent studies indicate that short episodes of hypotension may induce severe brain ischaemia, that will be present even after complete systemic haemodynamic restoration. The treatment of hypotensive episodes should be immediate and aggressive. In some circumstances, restoration of an adequate cerebral perfusion pressure may not be obtained sufficiently rapidly with fluids alone and may require early use of vasopressors. Optimal haemodynamic resuscitation of the trauma patient with haemorrhagic hypotension and severe head injury remains a special challenge.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Concept of secondary cerebral injury of systemic origin]. 767 75


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