Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms and potential mediator of hypercapneic pulmonary hypertension are incompletely understood. We studied 18 dogs, anaesthetised and spontaneously breathing both room air and after the inhalation of a gas mixture containing 10% CO2, 20.9% O2, and 69.1% N2, to determine the role of histamine, serotonin, and acidaemia in pulmonary hypertension produced by hypercapnia. Hypercapnia increased the mean pulmonary artery pressure by 0.33 kPa (2.5 mmHg) while wedge pressure and pulmonary arteriolar resistance did not change. Cardiac output significantly increased, indicating that the pulmonary hypertensive effect of hypercapnia is mainly flow related. Neither chlorpheniramine nor methysergide had significant effects on hypercapneic pulmonary hypertension. The infusion of sodium bicarbonate corrected the pH; pulmonary artery pressure and cardiac output increased while pulmonary arteriolar resistance dropped, suggesting that the increased cardiac output masked the effect of pH on pulmonary arteriolar resistance. The lack of effect of chlorpheniramine or methysergide on pulmonary resistances indicates that the vasoconstrictive effect of increased hydrogen ion concentration which accompanies hypercapnia is attributable neither to histamine nor to serotonin release.
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PMID:Mechanisms of hypercapneic pulmonary hypertension. 2 1

Thirteen years' experience with home oxygen for patients with advanced chronic obstructive pulmonary disease are reviewed. Home oxygen is safe and relieves pulmonary hypertension and elevated RBC mass in some, but not all patients. Marked clinical improvement is the most important result of long-term home oxygen use, including reduced hospitalizations and return to gainful employment for a few patients. Chronic compensated carbon dioxide retention is well tolerated and adaptive in cases of severe chronic airflow obstruction. New oxygen concentrators are effective in correcting hypoxemia and may make home oxygen administration more convenient and less expensive.
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PMID:Outpatient oxygen therapy in chronic obstructive pulmonary disease. A review of 13 years' experience and an evaluation of modes of therapy. 10 79

A homogeneous sample of 14 patients with advanced chronic bronchitis and emphysema complicated by secondary polycythaemia and pulmonary hypertension was examined. Eight patients who were receiving long-term oxygen therapy (LTO2) for 15-20 h in the 24 h day showed a significantly faster, that is more normal, frequency of the dominant EEG activity and a higher level of arterial oxygenation when breathing air than six similar patients not receiving LTO2. Acute administration of oxygen (2 1/min) for 15 min did not change the EEG pattern in either group of patients. The frequency of the dominant EEG activity in all 14 patients showed a significant positive correlation with the arterial oxygen saturation and negative correlation with the level of polycythaemia. Occurrence of intermixed EEG show activity theta and delta was positively correlated both with hypoxaemia and hypercapnia. The results suggest that the LTO2 in patients with chronic ventilatory failure has a beneficial effect on cerebral function as measured by EEG.
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PMID:The effects of long-term oxygen therapy on the EEG in patients with chronic stable ventilatory failure. 49 89

Hemodynamic values obtained during right heart catheterization in about 35 patients with chronic bronchitis were compared with the same variables 3.3 years later (range, 2 to 5 years). In the group of 13 patients with mean pulmonary arterial pressure less than 20 mm Hg at the first catheterization, the average value was 15.8 mm Hg at rest and 25.2 mm Hg during moderate exercise at the first investigation, and 16.9 and 26.3 mm Hg, respectively at the second catherization; the changes were not significant. In the group of pulmonary hypertensive patients, the mean pulmonary arterial pressure was 27.0 mm Hg at rest and 44.1 mm Hg during moderate exercise at the first catheterization, and 26.8 and 38.9 mm Hg, respectively, at the second catheterization. Thus, even in this group, there was no deterioration in pulmonary hemodynamics, because there was no significant change in right or left filling pressure, or in cardiac output. There was, however, a marked decrease in systemic arterial pressure, which was significant in the group with pulmonary hypertension. This decrease in left ventricular afterload could be partly responsible for the stabilization of pulmonary hemodynamics, and it could be due to the peripheral vasodilating effect of hypoxia and hypercapnia.
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PMID:Pulmonary and systemic hemodynamic evolution in chronic bronchitis. 61 21

Twelve patients with predominantly obstructive type sleep apnea underwent cardiac catheterization, hemodynamic monitoring, and arterial blood gas analysis during wakefulness and sleep. Abnormalities during wakefulness included systemic hypertension in four of 12, exercise-induced mild pulmonary hypertension in five of 12, and alveolar hypoventilation in one. During sleep nine patients had cyclic elevations of arterial pressure with each apneic episode, exceeding 200 mm Hg systolic in three of 12. Pulmonary artery pressures increased in 10 of 12, exceeding 60 mm Hg systolic in five. Marked degrees of hypoxemia (arterial P02, less than 50 mm Hg in eight of 12) and moderate hypercapnia with respiratory acidosis were associated with these hemodynamic changes. Cyclic upper airway obstruction during sleep may result in hypercapnia, acidosis, and pronounced hypoxemia, which can lead to hemodynamic abnormalities during sleep. Sustained pulmonary hypertension and possibly systemic hypertension may follow. Tracheostomy is an effective therapy and is recommended to symptomatic patients who have predominantly obstructive apnea but no relievable anatomic cause of upper airway obstruction.
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PMID:Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep. 99 7

The first case of "idiopathic" persistence of the fetal cardiopulmonary circulatory pathway with survival after a prolonged course is documented by serial cardiac catheterizations. All previously reported infants have either markedly improved within the first week of life or subsequently died. This entity has been described in term infants with prenatal or perinatal distress who present with tachypnea and cyanosis from birth. The chest radiograph is remarkable for the absence of pulmonary parenchymal pathology and the hemoglobin and hematocrit are normal. Blood gas determinations indicate hypoxia and acidosis with or without hypercarbia. Cardiac catheterization and angiography reveal an anatomically normal heart with severe pulmonary hypertension, left ventricular pressure lower than right ventricular pressure, and right-to-left venoarterial shunting through the fetal channels (atrial and or ductal levels). It is postulated that this entity may result from antenatal factors that affect the pulmonary vasculature and its subsequent adjustment to extrauterine life. These factors may include abnormal intrauterine stress resulting in excessive hypertrophy of the pulmonary arteriolar smooth muscle, or abnormal pulmonary vascular responsiveness to the usual vasoactive stimuli before or after birth, or an immature or dysfunctioning enzyme system necessary for the normal decrease in pulmonary artery pressure.
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PMID:Persistence of the fetal cardiopulmonary circulatory pathway: survival of an infant after a prolonged course;. 116 63

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

To evaluate the role of certain plasma biosubstances on the development of pulmonary hypertension and shock during severe hypoxia, hypercapnia and acidosis, plasma renin activity (PRA), angiotensin II (ATII), angiotensin converting enzyme (ACE), TXB2 and 6-Keto-PGF1 alpha (the stable metabolites of TXA2 and PGI2) were assayed in blood from pulmonary artery and aorta in seven pigs. Pulmonary arterial pressure (PAP) was monitored via Swan-Ganz catheter. During hypoxic and hypercapnic ventilation, PaO2 dropped to 4.7 kPa, PaCO2 rose to 21.1 kPa, pH dropped to 6.82, PAP increased from 2.43 +/- 0.06 to 4.46 +/- 0.45 kPa when acidotic shock developed (all P less than 0.05). Meanwhile ATII levels rose (all P less than 0.05). PRA significantly increased during acidotic shock as compared with normal ventilation (P less than 0.02). ACE dropped significantly (P less than 0.05), TXB2 and 6-keto-PGF1 alpha showed no significant change before and after hypoxic and hypercapnic ventilation.
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PMID:[Plasma renin activity, angiotensin II, angiotensin converting enzyme, thromboxane A2 and prostacyclin I2 levels in pigs with severe hypoxia and hypercapnea and acidosis shock]. 132 48

We studied the effects of laparoscopic cholecystectomy on respiratory and hemodynamic function in eight adult pigs. Minute ventilation was adjusted to normalize baseline arterial blood gases, then fixed throughout carbon dioxide insufflation. A metabolic measurement cart recorded total CO2 excretion, oxygen consumption, and minute ventilation. Carbon dioxide pneumoperitoneum was maintained at a constant pressure of 15 mm Hg as cholecystectomy was performed. After 1 hour of insufflation, CO2 excretion increased from 115 +/- 10 mL/min to 149 +/- 9 mL/min but O2 consumption remained unchanged. The PaCO2 increased from 35 +/- 2 mm Hg to 49 +/- 3 mm Hg and arterial pH fell from 7.47 +/- 0.02 to 7.35 +/- 0.03. Systemic and pulmonary hypertension occurred and stroke volume dropped from 35.5 +/- 3.5 mL to 28.6 +/- 2.2 mL with compensatory tachycardia. Right atrial pressure remained unchanged as inferior vena cava pressure increased to reflect the intraperitoneal pressure. We conclude that CO2 pneumoperitoneum resulted in significant transperitoneal CO2 absorption, with secondary hypercapnia and acidemia. The accumulation of CO2 was also associated with an increase in systemic and pulmonary arterial pressure. Heart rate increased to compensate for the decreased stroke volume to maintain cardiac output.
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PMID:Intraperitoneal carbon dioxide insufflation and cardiopulmonary functions. Laparoscopic cholecystectomy in pigs. 138 6

Bilateral lung transplantation (BLT) is a recently described procedure based on two sequential single-lung transplantations (SLT), which are performed by a transverse sternobithoracotomy. It does not require either cardiac arrest or routine use of cardiopulmonary bypass (CPB). The intraoperative management of 10 patients suffering from end-stage pulmonary disease is reported. Implantation of the first graft is quite similar to a SLT. Problems encountered during this procedure (ie, hypoxemia, hypercapnia, or low cardiac output) were due to restricted pulmonary and cardiac reserve. Preoperative and intraoperative assessment of the recipient's respiratory and cardiac status was, therefore, of prime importance. Mild preoperative pulmonary hypertension, well-preserved right ventricular function, and removal of the less well-perfused lung limited these difficulties; no patient required partial CPB at this stage. During the second lung implantation, gas exchange was provided by the first grafted lung. Measurements of pulmonary vascular resistance (PVR), venous admixture (Qva/Qt), and dead space (VD/VT) assessed with the arterial-to-end-tidal CO2 difference were used to confirm the adequacy of perfusion and V/Q matching. In one patient, partial CPB was instituted because of surgical difficulty related to inadequate size matching of the lungs. In the other patients, first graft function was satisfactory and the second graft was implanted without CPB. With chest closure, PVR returned to nearly normal values (range, 57-293, mean 167 dynes.s.cm-5) and Qva/Qt increased (range, 3 to 36, mean 20%). This limited series demonstrates that CPB is optional during this procedure. Good selection of recipients and donors, good lung preservation methods, and a short duration of cold ischemia are essential to success.
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PMID:Anesthesia for bilateral lung transplantation without cardiopulmonary bypass: initial experience and review of intraoperative problems. 149 95


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