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

The presence of persistent arrhythmias was correlated with hypercarbia (end-tidal CO2 greater than or equal to 55 mm Hg for greater than or equal to 60 s). A continuous strip chart recording of oxygen saturation, a capnogram, and an electrocardiogram were obtained from 402 children. No episodes of arrhythmia occurred in 153 patients younger than 2 yr compared with 24 patients 2 yr of age or older (P = 0.0001). Older patients whose airways were managed via a mask had a higher incidence (13.2% [21 of 159 patients]) than tracheally intubated patients (3.3% [3 of 90 patients]) (P = 0.01). In older patients whose tracheas were intubated, hypercarbia was associated with arrhythmia in 1 of 20 hypercarbia episodes. Seven of 16 patients with hypercarbia, whose airways were managed via a mask, had an arrhythmia (P = 0.0014); in eight, arrhythmias were associated with light anesthesia; in seven, arrhythmias were not associated with either hypercarbia or light anesthesia. Arrhythmias developed in 13 of 55 patients 2 yr old or older whose airways were managed via a mask and who were undergoing orchiopexy or herniorrhaphy as compared with 1 of 30 tracheally intubated patients (P = 0.016). There was a higher incidence of arrhythmias during halothane anesthesia compared with that during all other techniques (P = 0.035). The authors conclude that the incidence of arrhythmias is extremely low in infants younger than 2 yr. Hypercarbia is associated with arrhythmias in pediatric patients whose airways are managed via a mask but not in patients whose tracheas are intubated.(ABSTRACT TRUNCATED AT 250 WORDS)
Anesth Analg 1991 Dec
PMID:Persistent cardiac arrhythmias in pediatric patients: effects of age, expired carbon dioxide values, depth of anesthesia, and airway management. 195 67

Activity was recorded from physiologically identified baroreceptor or chemoreceptor fibers in carotid sinus nerves of urethane-anesthetized spontaneously breathing rabbits. A carotid sinus area was vascularly isolated so that carotid sinus pressure and perfusion medium (Locke's solution or rabbit blood) could be controlled. The cervical sympathetic, vagus, and aortic depressor nerves were bilaterally cut to eliminate vagal and cardiopulmonary reflexes. Baroreceptor fibers could be divided into two groups: fibers with a mean firing threshold of 47.6 +/- 1.9 mm Hg and no activity below this threshold (37 fibers) and fibers that were active at low intrasinus pressures (18.1 +/- 2.2 impulses/sec at an intrasinus pressure of 0 mm Hg). The baroreceptor fibers that were spontaneously active at low pressures were also chemically sensitive: discharge rate was increased by 5-hydroxytryptamine (10 fibers, p less than 0.01), nicotine (10 fibers, p less than 0.01), or hypercapnia (13 fibers, p less than 0.001). The activity of baroreceptor fibers with a clear pressure threshold was usually decreased by hypercapnia (26 of 27 fibers, from 18.8 +/- 3.1 to 13.2 +/- 3.9 impulses/sec). Chemoreceptor fibers failed to respond to intrasinus pressure changes from 0 to 100 mm Hg (n = 25 fibers, p greater than 0.5) but were sensitive to chemical changes, as expected. Thus, there is a subset of baroreceptor fibers that, under certain conditions, is spontaneously active at very low intrasinus pressures and responds to changes in the chemical milieu.
Circ Res 1991 Dec
PMID:Low-pressure-sensitive baroreceptor fibers recorded from rabbit carotid sinus nerves. 195 80

The separate effects of hypoxia and hypercapnia on the force-velocity relation of rabbit myocardium were compared in 10 papillary or trabecular muscles superfused using control (95% O2-5% CO2), hypoxic (18% O2), and hypercapnic (20% CO2) physiological salt solutions. This level of hypoxia did not irreversibly damage the muscles and reduced peak isometric force by 53 +/- 11%. The level of hypercapnia was chosen to match the force depression (50 +/- 12%) produced by hypoxia. Multiple force-velocity points were measured by applying critically damped isotonic force steps at 90% of the time to peak isometric force and at the time to 50% peak isometric force. These points defined the force-velocity relation and maximum velocity of shortening, the extrapolated isometric force, and the maximum power of nonpotentiated and postextrasytolic potentiated contractions. Hypoxia and hypercapnia reduced maximum force and maximum power nearly equally. Maximum velocity of shortening decreased more during hypoxia (21 +/- 12%) than during hypercapnia (12 +/- 9%) (p less than 0.01). Postextrasystolic potentiation completely reversed the reduction of maximum velocity of shortening during hypercapnia but not during hypoxia. A 6% internal load could account for the reduction in maximum velocity of shortening during hypercapnia and all but 9% of the reduction in maximum velocity of shortening during hypoxia. The relative time course of the force-velocity relation was not altered by either hypoxia or hypercapnia. We conclude that hypercapnia reduces the effect of activation because increased activation (by postextrasystolic potentiation) restored the force-velocity relation and maximum velocity of shortening to control values.(ABSTRACT TRUNCATED AT 250 WORDS)
Circ Res 1991 Dec
PMID:Effects of hypoxia and hypercapnia on the force-velocity relation of rabbit myocardium. 195 81

We prospectively evaluated 20 patient admissions for severe exacerbation of childhood asthma at The Children's Hospital, Boston, to detect evidence of cardiotoxicity. Evidence of cardiotoxicity was found in all six patient admissions for which isoproterenol infusion was utilized. This included marked elevation of serum creatine phosphokinase isoenzyme (CPK-MB) levels and electrocardiogram abnormalities consistent with transient myocardial ischemia. Peak serum CPK-MB levels were significantly lower and electrocardiogram abnormalities were significantly less frequent during 14 patient admissions for which isoproterenol infusion was not utilized. Risk factors associated with cardiotoxicity included tachycardia, hypercapnia, acidosis, and intravenous isoproterenol therapy. We conclude that cardiotoxicity is not infrequent during therapy for severe exacerbations of childhood asthma. Electrocardiograms and measurement of serum CPK-MB levels are sensitive, useful, and readily obtained indicators of cardiotoxicity. Abnormalities of these studies may detect cardiotoxicity prior to the occurrence of more blatant or catastrophic manifestations of cardiotoxicity. We therefore recommend serial monitoring of serum CPK-MB levels and electrocardiograms for all children requiring an admission to the intensive care unit for management of severe asthmatic exacerbation.
Pediatrics 1991 Dec
PMID:Cardiotoxicity during treatment of severe childhood asthma. 164 Dec 99

We examined the efficiency of continuous transtracheal O2 insufflation (TOI) as a method of ventilation during cardiopulmonary resuscitation (CPR) in a canine model. The tip of the insufflation catheter was placed 1 cm above the carina. The effects of TOI at flow rates of 0.2, 0.5, and 1.0 l/kg per min during and after CPR were examined in dogs with induced ventricular fibrillation. During CPR, adequate oxygenation and ventilation were maintained with TOI at flow rates of 0.5 and 1.0 l/kg per min, but not at 0.2 l/kg per min. After CPR, TOI was adequate to maintain oxygenation, but not ventilation. TOI alone did not prevent post-CPR hypercarbia in successfully resuscitated animals. Still, this study suggests that TOI might be useful as a temporary measure for emergency ventilation during CPR, especially in situations such as upper airway abnormalities, when mask ventilation or endotracheal intubation is not feasible.
Resuscitation 1990 Dec
PMID:Transtracheal O2 insufflation (TOI) as an alternative method of ventilation during cardiopulmonary resuscitation. 196 48

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)
Nihon Kyobu Shikkan Gakkai Zasshi 1990 Dec
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.
Kekkaku 1990 Dec
PMID:[Tuberculosis sequelae: pathophysiological aspect (ventilation)]. 207 61

Rabbits were divided into 6 groups according to concentration of the test gases (O2-CO2-N2 gas mixture) used; 0%-5%-95%: 0% group, 1.0%-5.1%-93.9%: 1% group, 2.0%-10.3%-87.7% and 1.9%-20.6%-77.5%: 2% groups, 3.1%-5.1%-91.8%: 3% group, 4.1%-5.1%-90.8%: 4% group. In addition to the normocapnic groups, two hypercapnic groups (10% and 20% groups) were included. After an intravenous injection of urethane for anesthesia, the rabbit was fixed on its back on an operating table and the trachea was cannulated. Animals inhaled the test gases through a cylindrical unidirectional valve box connected to the cannula. Blood samples were drawn from the catheterized femoral artery. The length of time to the onset of apnea became shorter as the O2 concentration became lower. The 0%, 1%, and 20% CO2-added 2% groups became apneic within 1 min. The effect of severe hypercapnia was marked. The 20% CO2 group became apneic much sooner than the 10% CO2 group. The onset of apnea was much later in the 3% and 4% groups, and in these groups a steady state PO2-level was observed. The PO2 values in the steady state were 17 mmHg for the 3% group and 21 mmHg for the 4% group. The PO2 value at apnea was about 10 mmHg in the O%, 1%, and 10% CO2-added 2% groups. The effect of severe hypercapnia on this variable was also observed, the value in the 20% group being 15.8 mmHg. Apnea ensued immediately following a strong inspiratory effort which was diagnosed as apneusis.(ABSTRACT TRUNCATED AT 250 WORDS)
Nihon Hoigaku Zasshi 1990 Dec
PMID:The interaction between severe hypercapnia and hypoxia. 212 13

The hemodynamic effects of high arterial carbon dioxide pressure (PaCO2) during anesthesia in horses were studied. Eight horses were anesthetized with xylazine, guaifenesin, and thiamylal, and were maintained with halothane in oxygen (end-tidal halothane concentration = 1.15%). Baseline data were collected while the horses were breathing spontaneously; then the horses were subjected to intermittent positive-pressure ventilation, and data were collected during normocapnia (PaCO2, 35 to 45 mm of Hg), moderate hypercapnia (PaCO2, 60 to 70 mm of Hg), and severe hypercapnia (PaCO2, 75 to 85 mm of Hg). Hypercapnia was induced by adding carbon dioxide to the inspired gas mixture. Moderate and severe hypercapnia were associated with significant (P less than 0.05) increases in aortic blood pressure, left ventricular systolic pressure, cardiac output, stroke volume, maximal rate of increase and decrease in left ventricular pressure (positive and negative dP/dtmax, respectively), and median arterial blood flow, and decreased time constant for ventricular relaxation. These hemodynamic changes were accompanied by increased plasma epinephrine and norepinephrine concentrations. Administration of the beta-blocking drug, propranolol hydrochloride, markedly depressed the response to hypercapnia. This study confirmed that in horses, hypercapnia is associated with augmentation of cardiovascular function.
Am J Vet Res 1990 Dec
PMID:Hemodynamic effects of carbon dioxide during intermittent positive-pressure ventilation in horses. 212 72

Response to CO2 and autoregulation of cortical cerebral blood flow (CBF) during isoflurane anesthesia were studied in 10 patients undergoing neurosurgery. The patients were anesthetized with 0.5 to 1.2% end-tidal isoflurane and 66% nitrous oxide in oxygen. The CBF was measured by thermal diffusion using a flow probe with a Peltier stack. PaCO2 was controlled to produce hypocarbia, normocarbia and hypercarbia by changing tidal volume and respiratory rate. Arterial blood pressure was altered. Hypotension was achieved by intravenous infusion of trimetaphan and hypertension was induced by intravenous administration of metaraminol. During isoflurane anesthesia the response to CO2 of CBF was kept at PaCO2 between 27.8 and 53.9 mmHg. The following relationship was obtained. CBF = 2.54 x PaCO2-53.0, r = 0.59, n = 131 The autoregulation of CBF was evaluated in 7 patients, and in 2 patients, the autoregulation of CBF was abolished.
Masui 1990 Dec
PMID:[Response to CO2 and autoregulation of cortical cerebral blood flow during isoflurane anesthesia]. 212 31


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