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At least 523 records · Page 29Linked to original sources
PubMed1995

Treatment of respiratory failure due to kyphoscoliosis with nasal intermittent positive pressure ventilation (NIPPV).

Nasal intermittent positive pressure ventilation (NIPPV) represents a major advance in the management of respiratory failure. While its role in chronic respiratory failure is well documented, its use in acute respiratory failure is less well defined. We studied four patients with respiratory failure due to kyphoscoliosis, two of whom presented with acute respiratory acidosis. All four patients were on conventional maximum medical therapy prior to treatment with NIPPV. All patients survived to be discharged from hospital on home ventilation and significant improvements were noted in pO2, pCO2 and pulmonary function. We conclude that NIPPV is useful in the management of both acute and chronic ventilatory failure due to kyphoscoliosis.

Acidosis, Respiratory↗
PubMed2007

Perioperative extracorporeal membrane oxygenation support for critical pediatric airway surgery.

Extracorporeal membrane oxygenation (ECMO) has been used for cardiopulmonary support in neonates, infants, and adults. We report the application of ECMO for critical airway surgery when mechanical ventilation cannot provide adequate gas exchange. Three pediatric patients underwent emergency ECMO establishment because of hypercapnia that could not be managed by conventional mechanical ventilation. The pathology included: (1) left pulmonary artery sling with long-segment tracheal stenosis; (2) absence of the right intermediate bronchus and abnormal origin of the right lower bronchus arising from the left main bronchus; (3) right-lung agenesis with long-segment tracheobronchial stenosis. Venoarterial ECMO was established. Before ECMO, the arterial pH values were 7.28, 7.0, and 7.08, and the PaCO2 values were 111.8, 112.0, and 208.7 mmHg for each patient, respectively. After ECMO support, respiratory acidosis was reversed. The patients then underwent surgical intervention. The surgical procedures included: (1) slide tracheoplasty and reimplantation of the left pulmonary artery; (2) resection of the stenotic tracheal segment and reconstruction of the bronchial tree; (3) tracheal dilatation and stent implantation. The ECMO durations were 11, 5, and 16 h, respectively. All patients were successfully weaned off ECMO without complications. In conclusion, ECMO provided adequate ventilation support for patients undergoing critical tracheobronchial reconstruction when conventional mechanical ventilation could not maintain adequate gas exchange.

Acidosis, Respiratory↗
PubMed1983

Ketamine, catecholamines, and uterine tone in pregnant ewes.

Blood levels of ketamine, measured in both mother (1,230 ng/ml at 1 minute) and fetus (470 ng/ml at 1 minute) illustrate not only rapidly decreasing levels of the drug after its intravenous administration but also its transplacental passage. Concentrations of norepinephrine, epinephrine, and dopamine did not change in the mother or fetus after ketamine, with the exception of maternal levels of epinephrine, which were significantly higher at 45 minutes than control values (p less than 0.05). Maternal effects of ketamine consisted of increases in mean arterial pressure (7% p less than 0.05), cardiac output (16% p less than 0.01), and respiratory acidosis, all of which were slight and transitory. Although resting uterine tone increased (39% p less than 0.01), the uterine blood flow remained constant. None of the physiologic alterations could be correlated with changes in catecholamine levels. Therefore, the cardiovascular and uterine stimulating properties of ketamine at a dose of 0.7 mg/kg are small and are not the result of increased catecholamine levels in plasma. Further studies are necessary to elucidate the mechanism.

Acidosis, Respiratory↗
PubMed1984

Effect of carbonic anhydrase inhibition on the DC potential difference between cerebrospinal fluid and blood.

The effect of cerebral carbonic anhydrase inhibition on the DC potential difference between cerebrospinal fluid (CSF) and blood (PD) was studied in anesthetized dogs by perfusing the ventriculocisternal system with artificial CSF containing the carbonic anhydrase inhibitor, acetazolamide. The slope of the PD vs. arterial blood pH (delta PD/delta pHa) was calculated from PD and pHa values obtained during room-air breathing, respiratory acidosis, and respiratory alkalosis. delta PD/delta pHa decreased from -26.3 +/- 1.9 millivolts per pH unit (mV/U) before acetazolamide administration to 17.6 +/- 2.1 after acetazolamide (P less than 0.02). The PD at pH 7.4 (PD7.4) increased slightly from 2.9 +/- 0.5 mV before acetazolamide treatment to 3.9 +/- 0.6 after acetazolamide (P less than 0.02). The results suggest that carbonic anhydrase could be involved in generating the PD between CSF and blood.

Acetazolamide↗
PubMed1984

Acid-base and ventilatory adaptation in conscious dogs during chronic hypercapnia.

Ventilation and cisternal cerebrospinal fluid (CSF) and arterial acid-base balance were measured in awake dogs during air control and from 1 h to 26 days of breathing 5% CO2 in air. Ventilation increased 4-fold during acute hypercapnia and then declined to a minimum at 5-10 days. Between 1-3 days and 16-26 days of hypercapnia ventilation was relatively stable at 2.5 times control. [HCO3-]CSF increased rapidly by 12 h of hypercapnia and in the steady-state [HCO3-]CSF was correlated with PCSFCO2. Between 1 h and 1.5 days of hypercapnia, increase in [HCO3-]CSF was also correlated with increase in [NH3]CSF. Despite increase in [HCO3-]CSF, there was no compensation of [H+]CSF throughout 26 days of hypercapnia. Hydrogen ion may have contributed to the control of ventilation during chronic hypercapnia since ventilation was correlated with [HCO3-]a and [HCO3-]CSF. However, a relationship between ventilation and [H+] of arterial blood and CSF during chronic hypercapnia was relatively poor or absent. Ventilatory adaptation to chronic hypercapnia could not be related to metabolism or to [NH3]CSF. The mechanism(s) by which the increase in PCO2 during chronic respiratory acidosis results in sustained elevation of ventilation remains to be resolved.

Acid-Base Equilibrium↗
PubMed1987

Transmission fatigue of the rabbit diaphragm.

This study evaluates the role of transmission fatigue of the diaphragm in rabbits subjected to inspiratory resistive loading (IRL) sufficiently severe to increase peak tidal airway pressure to about 50% of that elicited by 100 Hz phrenic nerve stimulation. After 58 +/- 14 min of IRL, the transdiaphragmatic pressure (Pdi) responses to phrenic nerve stimulation at 20, 60, and 100 Hz were reduced by approximately one third. In contrast, IRL induced no significant change in the response to direct diaphragm stimulation (in the presence of transient neuromuscular blockade). Although respiratory acidosis occurred during IRL (pH 7.04 +/- 0.04, PCO2 90 +/- 10, PO2 131 +/- 38), it was not sufficient to explain the reduced contractility. In a separate series of experiments, the diaphragm compound action potential elicited by unilateral phrenic nerve stimuli was recorded by implanted diaphragm electrodes and the Pdi elicited by contralateral phrenic nerve stimulation at 100 Hz was measured. Both action potential amplitude and Pdi declined during IRL and both improved after 10 min of recovery. These findings demonstrate that transmission fatigue plays a major role in rabbit diaphragm fatigue induced by spontaneous breathing against inspiratory resistance.

Acidosis, Respiratory↗
PubMed1990

Bumetanide and cerebrospinal fluid acid-base variables during acute CO2 elevation.

The purpose of this study was to investigate the effects of bumetanide, an inhibitor of NaCl cotransport on cisternal cerebral spinal fluid (CSF) acid-base balance during acute respiratory acidosis (ARA). We measured blood and CSF acid-base variables in two groups (N = 7 in each) of anesthetized paralyzed and mechanically ventilated dogs with bilateral ligation of renal pedicles (to eliminate saluresis). After baseline samples were obtained (-1 h) bumetanide (0.5 mg/kg) was administered intravenously within 15 min (group 2); group 1 received equal volume of diluted saline. ARA was induced 1 h later (0 h) and was maintained for 5 h. In both groups PaCO2 was maintained between 55 to 60 mm Hg. Mean cisternal CSF PCO2 was 42.8 +/- 2.6, and 43.8 +/- 2.5 mm Hg, respectively in group 1 and group 2 and rose approximately 20 mm Hg during ARA. In group 1, CSF [HCO3-] was 22.0 +/- 1.0, 24.8 +/- 0.6, and 25.4 +/- 1.6 mEq/L, respectively at 0, 2 1/2, and 5 h; respective values for group 2 were 22.9 +/- 1.5, 24.7 +/- 1.4, and 26.1 +/- 1.3 mEq/L. Comparing the two groups, respective values were not significantly different from each other. Similarly, between the two groups changes in CSF [Na(+)-Cl-] during ARA were not significantly different from each other. Based on our results we conclude that at the dose used in the present study bumetanide does not change ionic composition and acid-base balance of cisternal CSF when compared to controls. Because changes in CSF [Na(+)-Cl-] during ARA were similar in both groups, any inhibition of Cl- influx into CSF by bumetanide should have been proportional to that of Na+.

Acid-Base Equilibrium↗
PubMed1980

Evidence that respiratory depression by serotonin agonists may be exerted in the central nervous system.

Resting with CO2 stimulated respiration were measured by means of a whole body plethysmograph in rats lightly anesthetized with halothane. The respiratory effects of different doses of the serotonin precursor 5-HTP, and the serotonin agonist 5-methoxy-N,N-dimethyltryptamine were studied as well as the effects of a serotonin antagonist methysergide and p-chlorophenylalanine, an inhibitor of serotonin synthesis. The serotonergic agonists decreased tidal volume and minute volume in a dose dependent manner and produced a respiratory acidosis. The respiratory depressant effect was antagonized by methysergide, and the serotonergic antagonist and synthesis inhibitor alone stimulated respiration. Rats given intraventricular 5-methoxy-N,N-dimethyltryptamine also evidenced a decrease in tidal volume, and this response was greater in animals given 5,7-dihydroxytryptamine. It seems likely that CNS serotonin receptors are involved in the control of both basal and CO2 stimulated respiration.

5-Hydroxytryptophan↗
PubMed2006

Control of rectal gland secretion by blood acid-base status in the intact dogfish shark (Squalus acanthias).

In order to address the possible role of blood acid-base status in controlling the rectal gland, dogfish were fitted with indwelling arterial catheters for blood sampling and rectal gland catheters for secretion collection. In intact, unanaesthetized animals, isosmotic volume loading with 500 mmol L-1 NaCl at a rate of 15 mL kg-1 h-1 produced a brisk, stable rectal gland secretion flow of about 4 mL kg-1 h-1. Secretion composition (500 mmol L-1 Na+ and Cl-; 5 mmol L-1 K+; <1 mmol L-1 Ca2+, Mg2+, SO(4)2-, or phosphate) was almost identical to that of the infusate with a pH of about 7.2, HCO3- mmol L-1<1 mmol L-1 and a PCO2 (1 Torr) close to PaCO2. Experimental treatments superimposed on the infusion caused the expected disturbances in systemic acid-base status: respiratory acidosis by exposure to high environmental PCO2, metabolic acidosis by infusion of HCl, and metabolic alkalosis by infusion of NaHCO3. Secretion flow decreased markedly with acidosis and increased with alkalosis, in a linear relationship with extracellular pH. Secretion composition did not change, apart from alterations in its acid-base status, and made negligible contribution to overall acid-base balance. An adaptive control of rectal gland secretion by systemic acid-base status is postulated-stimulation by the "alkaline tide" accompanying the volume load of feeding and inhibition by the metabolic acidosis accompanying the volume contraction of exercise.

Acid-Base Equilibrium↗
PubMed1996

Effect of subcutaneous carbon dioxide insufflation on arterial pCO2.

PURPOSE: Subcutaneous emphysema following laparoscopy could result in postoperative respiratory acidosis from prolonged CO2 absorption. We studied the magnitude and duration of alterations in PaCO2 coincident with direct CO2 insufflation into the subcutaneous fat of the anterior abdominal wall of 5 anesthetized juvenile pigs. METHODS: First, each pig was insufflated with 6 L of CO2 to produce moderate emphysema over the trunk. Following return to baseline PaCO2, each pig was re-insufflated with 12 L of CO2 to produce severe emphysema over lower limbs, neck, head, and trunk. Measurements of arterial blood gases were performed every 5 or 10 min. Minute ventilation was held constant to represent the worst case scenario. RESULTS: From baseline PaCO2 of 41.8 +/- 2.3 mm Hg, PaCO2 peaked at 68.3 +/- 8.6 (P < 0.02) and 92.9 +/- 10.7 (P < 0.01) mm Hg for the 6- and 12-L volumes, respectively, 20 to 25 minutes following insufflation. From baseline arterial pH of 7.40 +/- 0.02, respective nadirs of pH were 7.21 +/- 0.06 (P < 0.02) and 7.08 +/- 0.05 (P < 0.01). PaCO2 and arterial pH took approximately 100 minutes to return to baseline after insufflation with both 6 and 12 L volumes. CONCLUSIONS: When minute ventilation is fixed, subcutaneous CO2 insufflation causes increased PaCO2 and decreased pH that may persist for a prolonged period of time. Therefore, patients with subcutaneous emphysema after laparoscopy should be observed in postanesthetic recovery until PaCO2 and pH approach baseline.

Abdominal Muscles↗
PubMed1984

End-tidal CO2 and tissue pH in the monitoring of acid-base changes: a composite technique for continuous, minimally invasive monitoring.

The infrared CO2 analyzer continuously monitors the CO2 tension in exhaled air at end-tidal expiration. In experimental animals, we found a consistent relationship between PaCO2 and end-tidal CO2 (ET.CO2) in the normal steady state, and in acid-base disturbances (respiratory acidosis and alkalosis, and hypoperfusion acidosis). Paired data analyses of PaCO2 (X) and ET.CO2 (Y) yielded correlation coefficients of r = 0.98 (Y = 0.96X + 4.43) during progressive hypercarbia (PaCO2: 32----110 torr), and r = 0.93 (Y = 0.89X + 0.93) during hyperventilation hypocapnia (PaCO2: 41----14 torr). The relationship between PaCO2 and ET.CO2 was seen during hypovolemic shock if pulmonary perfusion was maintained uniform in all areas of lung. The ability of the ET.CO2 sensor to predict instantaneously the PaCO2 makes it attractive enough to be used in conjunction with the subcutaneous tissue pH(pHe) sensor in the management of acid-base disturbances. After hypercarbia (FiCO2 0.15 X 40 min; PaCO2/ET.CO2: 100/101 torr), when the dogs were returned to room air, abruptly both the ET.CO2 and pHe sensors were sensitive to the changes in Fi.CO2. But the response of the ET.CO2 was swifter. The advent of transcutaneous gas monitors has shown that intermittent blood gas analyses, however frequent, are inadequate for the monitoring of the rapidly altering blood gas status in the acutely ill. The ability of the pHe sensor to identify whole-body acidosis and alkalosis combined with the speed and ease of the ET.CO2 monitor in pinpointing hypercarbic and hypocarbic states makes this two-parameter system suitable for the continuous, noninvasive monitoring of the critically ill.

Acidosis, Respiratory↗
PubMed1977

Studies in acid-base balance. I. Effect of alkali therapy in newborn dogs with mechanically fixed ventilation.

The effect of rapid or slow infusion of hypertonic sodium bicarbonate on acid-base balance and serum osmolality was studied in 36 acidotic newborn dogs. Respiratory acidosis and hypoxia were produced by mechanically fixed hypoventilation. One group of animals breathed 100% O2 to prevent hypoxemia. Rapid infusion of HCO3- in acidotic and hypoxic animals resulted in only a transient (1 minute) and small (0.05 pH units) elevation of arterial pH followed by a continuous fall, resulting in a lower pH and a worsened metabolic condition than in the nontreated controls. In nonhypoxic acidotic animals, rapid infusion of HCO3- had little effect on arterial pH. PaCO2 increased suddenly by 17 Torr in hypoxic and, by 13 Torr, in nonhypoxic animals. There was a concomitant fall in PaO2 (15 Torr). Serum osmolality rose rapidly after rapid infusion of HCO3-. Rapid infusion of hypertonic bicarbonate into an animal or infant whose ventilation is fixed thus results in a less than predicted elevation of arterial pH. PaCO2 rises, PaO2 falls, and serum osmolality rises. The net result may be a worsening rather than an improvement in the animals' metabolic state.

Acid-Base Equilibrium↗
PubMed1985

Furosemide decreases ventilation in young rabbits.

To test the hypothesis that furosemide would cause metabolic alkalosis and thus alveolar hypoventilation, normal rabbit pups were given either furosemide (4 mg/kg/day) or saline solution for the first 8 to 10 days of life. Pups given furosemide developed primary metabolic alkalosis and reduced ventilation, which resulted in secondary respiratory acidosis. Lung compliance was improved by furosemide, and the ventilatory response to CO2 was unaffected. KCl injection in alkalotic pups increased ventilation and decreased pH. The data show that conventional doses of furosemide can (1) cause metabolic alkalosis and reduce ventilation; (2) increase the PaCO2, which reflects changes in acid-base status and not changes in lung function; and (3) increase lung compliance, perhaps by decreasing lung water. When these effects occur in infants with chronic lung disease, the beneficial effect of furosemide may be obscured.

Acidosis, Respiratory↗
PubMed2001

Respiratory acid-base disorders.

Respiratory acid-base disorders, although infrequently diagnosed in veterinary medicine, can cause or contribute to adverse clinical outcomes. Recognition of the mechanisms and causes of respiratory acidosis and alkalosis can prompt clinical detection of the acid-base derangement, allowing for appropriate intervention.

Acidosis, Respiratory↗
PubMedDate not supplied

Clonidine and sleep apnea syndrome interaction: antagonism with yohimbine.

A patient with sleep apnea syndrome, concurrently taking clonidine as an antihypertensive, presented with severe respiratory acidosis, hypotension, and associated central nervous system depression. Acidosis was improved by mechanical ventilation, and central nervous system (CNS) depression and hypotension were reversed with yohimbine. Clonidine may have an additive CNS depressive effect in sleep apnea syndrome and should be used with caution in such patients. Yohimbine's sympathetic-enhancing effects may be useful in clonidine toxic states.

Acidosis, Respiratory↗
PubMed1996

[Hemodynamic changes induced by apnea test in patients with brain death].

OBJECTIVE: In France, an apnoea test is compulsory to confirm brain death. This test results in a major hypercarbia and respiratory acidosis. This study aimed to assess haemodynamic changes elicited by the apnoea test. STUDY DESIGN: Prospective clinical study. PATIENTS: Fifteen patients with brain death METHODS: Before the apnoea test, the lungs were ventilated with pure oxygen for 20 minutes. Thereafter, the test was conducted with continuous oxygen flow through the endotracheal tube, and SpO2 monitoring. Blood gases and haemodynamic parameters, including systemic arterial pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, cardiac index and right ventricular function parameters were assessed before, during and 20 minutes after the apnoea test. Mean values at the various times were compared. RESULTS: Hypercarbia and acidosis induced a major pulmonary hypertension and an increase in cardiac output, associated with a decrease in systemic vascular resistances. Despite pulmonary hypertension and acidosis, right ventricular function was maintained. All haemodynamic modifications were reversed by reventilation. CONCLUSION: Apnoea test induces a reversible pulmonary hypertension that is seemingly not deleterious for right ventricular function. Apnoea test probably does not alter viability of the donor's organs.

Acidosis, Respiratory↗
PubMed2000

The art of building decision trees.

Decision support systems that help physicians are becoming a very important part of medical decision making. They are based on different models and the best of them are providing an explanation together with an accurate, reliable, and quick response. One of the most viable among models are decision trees, already successfully used for many medical decision-making purposes. Although effective and reliable, the traditional decision tree construction approach still contains several deficiencies. Therefore we decided to develop and compare several decision support models using four different approaches. We took statistical analysis, a MtDeciT, in our laboratory developed tool for building decision trees with a classical method, the well-known C5.0 tool and a self-adapting evolutionary decision support model that uses evolutionary principles for the induction of decision trees. Several solutions were evolved for the classification of metabolic and respiratory acidosis (MRA). A comparison between developed models and obtained results has shown that our approach can be considered as a good choice for different kinds of real-world medical decision making.

Acidosis, Respiratory↗
PubMed1990

Stability of brain intracellular lactate and 31P-metabolite levels at reduced intracellular pH during prolonged hypercapnia in rats.

The tolerance of low intracellular pH (pHi) was examined in vivo in rats by imposing severe, prolonged respiratory acidosis. Rats were intubated and ventilated for 10 min with 20% CO2, for 75 min with 50% CO2, and for 10 min with 20% CO2. The maximum PaCO2 was 320 mm Hg. Cerebral intracellular lactate, pHi, and high-energy phosphate metabolites were monitored in vivo with 31P and 1H nuclear magnetic resonance (NMR) spectroscopy, using a 4.7-T horizontal instrument. Within 6 min after the administration of 50% CO2, pHi fell by 0.57 +/- 0.03 unit, phosphocreatine decreased by approximately 20%, and Pi increased by approximately 100%. These values were stable throughout the remainder of the hypercapnic period. Cerebral intracellular lactate, visible with 1H NMR spectroscopy in the hyperoxic state, decreased during hypercapnia, suggesting either a favorable change in oxygen availability (decreased lactate production) or an increase in lactate clearance or both. All hypercapnic animals awakened and behaved normally after CO2 was discontinued. Histological examination of cortical and hippocampal areas, prepared using a hematoxylin and eosin stain, showed no areas of necrosis and no glial infiltrates. However, isolated, scattered, dark-staining, shrunken neurons were detected both in control animals (no exposure to hypercapnia) and in animals that had been hypercapnic. This subtle histological change could represent an artifact resulting from imperfect perfusion-fixation, or it could represent subtle neurologic injury during the hypercapnia protocol. In summary, extreme hypercapnia and low pHi (approximately 6.5) are well tolerated in rats for periods up to 75 min if adequate oxygenation is maintained.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗