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PubMed1980

Response of the collecting duct to disturbances of acid-base and potassium balance.

With light microscopy and scanning electron microscopy, the epithelium of the collecting duct was examined in rats with acute and chronic acid-base disturbances, hypokalemia, hyperkalemia, and during osmotic diuresis and hydropenia. Acid-base disturbances included acute respiratory acidosis, acute metabolic alkalosis, and chronic metabolic acidosis. Two groups of hypokalemic animals were studied, those with and those without an associated metabolic alkalosis. After the appropriate physiologic data were collected, all kidneys were preserved for morpholigic data were collected, all kidneys were preserved for morphologic evaluation by in vivo intravascular perfusion fixation. The percentage of intercalated cells in the epithelium of the collecting duct in the cortex and outer medulla of each kidney was determined by light microscopic examination of 1-mu-thick Epon sections stained with toluidine blue. Qualitative observations were performed with scanning electron microscopy. Intercalated cells represented 36 to 40% of the epithelial cells forming the collecting duct in the cortex and outer and inner stripes of the outer medulla in control animals during hydropenia and during mild osmotic diuresis. No experimental condition studied was found to influence significantly the actual or relative number of intercalated cells, or their distribution in the collecting duct. The hypertrophy of both principal cells and intercalated cells in potassium-depleted animals occurred in both the presence and the absence of metablic alkalosis. Conclusion. Under the conditions of this study, intercalated cells represent a constant population of epithelial cells in the rat collecting duct, and intercalated and principal cells represent distinct cell typs, each defined by rather constant morphologic features. Contrary to previous reports, no evidence was found that a disturbance of hydrogen ion and potassium balance is associated with a conversion of principal to intercalated cells in the collecting duct.

Acid-Base Imbalance↗
PubMed1985

Regulation of acid-base equilibrium in chronic hypercapnia.

Previous studies from this laboratory have demonstrated that the decreased renal bicarbonate reabsorption prevailing during chronic hypocapnia is not mediated by the alkalemia that normally accompanies this acid-base disturbance but by some direct consequence of the change in PaCO2 itself. Based on the reasonable expectation that the mechanisms underlying the kidney's response to primary respiratory disturbances would be similar over the entire spectrum of physiologic carbon dioxide tensions, the present study was designed to assess whether an acidic change in systemic pH is a critical factor in the renal response to chronic hypercapnia. For this purpose, the plasma and renal responses to chronic respiratory acidosis in normal dogs were compared to those in dogs chronically fed a large hydrochloric acid (HCl) load (7 mmoles/kg/day). Exposure to 6% carbon dioxide for 7 days in a large environmental chamber induced a stable increment in PaCO2 which averaged 17 +/- 0.5 and 22 +/- 1.3 mm Hg in normal and HCl-fed animals, respectively. Steady-state plasma bicarbonate concentration rose from 22.0 +/- 0.4 to 27.1 +/- 0.5 mEq/liter in normals and from 14.7 +/- 0.7 to 24.2 +/- 0.8 mEq/liter in the HCl-fed group. As a result of these changes in PaCO2 and plasma bicarbonate, steady-state plasma hydrogen ion concentration rose in normals from 41 +/- 0.8 to 49 +/- 0.9 nEq/liter (pH 7.39 +/- 0.01 vs. 7.31 +/- 0.01) but did not change significantly in the HCl-fed group (55 +/- 1.4 vs. 56 +/- 1.4 nEq/liter; pH 7.26 +/- 0.01 vs. 7.25 +/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1993

Acid-base significance of meconium discovered prior to labor.

Although the significance of meconium in the amniotic fluid diagnosed during labor remains problematic, there is little information regarding the significance of meconium discovered prior to labor. The present study consisted of 40 term pregnancies with meconium found at amniocentesis for lung maturity (n = 7) or elective cesarean section (n = 33) and 40 uncomplicated, control pregnancies with clear amniotic fluid at elective cesarean section. The mean umbilical artery (UA) blood pH was 7.26 in the meconium group and 7.28 in the control group. Overall, the frequency of fetal acidemia (UA pH < 7.20) was 15% (6 of 40) of the infants in the meconium group versus 8% (3 of 40) in the control group (p = 0.24). All nine of these infants had a respiratory acidosis defined as a UA blood pH less than 7.20 with normal bicarbonate and elevated carbon dioxide pressure. Importantly, none of the neonates had metabolic acidemia and all had uncomplicated hospital courses. All of the pregnancies reported were promptly delivered because of meconium and we therefore cannot recommend nonintervention when meconium is diagnosed in the antepartum period. Meconium discovered prior to labor is not necessarily a marker of immediate or chronic fetal compromise.

Acid-Base Equilibrium↗
PubMed2000

Effect of carbon dioxide on cochlear blood flow in guinea pigs.

The influence of carbon dioxide (CO2) on cochlear blood flow (CBF), blood pressure (SBP) and skin blood flow (SBF) was studied in anaesthetized guinea pigs. A transient acute respiratory acidosis was produced by inhalation of CO2 and oxygen (O2) gas mixtures. The blood flows were measured by laser Doppler flowmetry (LDF). High CO2 increased CBF and SBP, and decreased SBF in a dose-dependent manner. The responses of CBF, SBP and SBF to high CO2 were reversible. Our results indicate that high CO2 (and low pH) dilates the smooth muscle of the blood vessels, resulting in an increase in CBF. CO2 also activates the sympathetic nervous system in the whole body, producing an increase in SBP. The distribution of alpha-adrenergic fibres receptors is abundant in skin and scarce in the cochlea. The constrictive effect on blood vessels is much greater in the skin than in the cochlea, thus our results showed a decrease in SBF during stimulation with higher CO2.

Acidosis, Respiratory↗
PubMed1979

Balance of net base in the rat: adaptation to and recovery from sustained hypercapnia.

Net base and mineral balances were evaluated in a group of male 350 g Wistar rats exposed to 10% carbon dioxide in air for 10 days with a view to identifying the source of net base subject to retention during renal compensation of sustained respiratory acidosis. In response to hypercapnia, the rate of renal net acid excretion rose but insignificantly. However, a rise in whole body net base concentration from about 215 mmol/kg to about 250 mmol/kg came about by ongoing gastrointestinal absorption in the weight-losing animal, absorbed net base being distributed to extracellular and non-extracellular compartments of the body, presumably including bone. During an 8-day recovery period, a small decrement in whole body net base concentration was observed.

Acid-Base Equilibrium↗
PubMed2005

Halothane, an effective infrequently used drug, in the treatment of pediatric status asthmaticus: a case report.

Asthma is the most common chronic disease of childhood. Despite a better understanding of the disease process and its management, status asthmaticus continues to be a life-threatening event. The use of volatile inhaled anesthetics is infrequently reported as adjunctive therapy to conventional treatment of this condition. We report the use of halothane in a mechanically ventilated pediatric patient with life-threatening status asthmaticus who was admitted to the pediatric intensive care unit (PICU) after failing to respond to standard medical therapy and noninvasive positive pressure ventilation. A 12-year-old African American male was seen in the emergency department and treated with intravenous corticosteroids, beta-agonist therapy. He deteriorated rapidly and required endotracheal intubation and mechanical ventilation. Two hours later, the patient developed an acute, severe respiratory acidosis (pH=6.97, PaCO2=171, PaO2=162, BE=1.7). Halothane was started at 2% by using the Siemens Servo 900C anesthesia ventilator. Improvement in both arterial blood gases and exhaled tidal volume were noted 30 minutes after initiation of the anesthetic gas. The patient remained on halothane for a total of 36 hours. No adverse effects associated with the use of halothane were noted. The patient was extubated to BiPAP 16/6, FiO2=0.30 at 68 hours and was discharged home 5 days later.

Acidosis, Respiratory↗
PubMed1991

Prospective analysis of cardiopulmonary responses to laparoscopic cholecystectomy.

This prospective study evaluates the extent and temporal course of the cardiorespiratory effects of CO2 during laparoscopic cholecystectomy in otherwise healthy patients. Sixteen patients (M:F = 3:13, average age = 40.2 +/- 14.1 years) were monitored with capnography, transesophageal cardiac output, continuous blood pressure, heart rate, and pulse oximetry. Arterial blood gases were obtained immediately before insufflation of the abdomen with CO2 and before desufflation. Average operative time was 137 +/- 13 minutes. Patients were paralyzed and mechanically ventilated. Minute ventilation was increased if EtCO2 exceeded 45 mmHg or rose by more than 12 mmHg from baseline. End tidal (EtCO2) and arterial CO2 (PaCO2) increased from 31.4 +/- 0.7 mmHg to 42.1 +/- 1.6 mmHg and 33.3 +/- 0.7 mmHg to 43.7 +/- 1.2 mmHg, respectively, during the course of the procedure. Arterial pH decreased from 7.43 +/- 0.01 to 7.34 +/- 0.01, while bicarbonate concentration remained unchanged. Thirteen of the 16 patients required increased minute ventilation due to hypercarbia detected by capnography. Blood pressure increased from 78 +/- 2 mmHg (mean) at the start to 98 +/- 2 mmHg. This increase was coincidental with the maximal PaCO2. Good agreement was observed between paired EtCO2 and PaCO2 measurements. Laparoscopic cholecystectomy with carbon dioxide insufflation causes significant respiratory acidosis and associated cardiovascular changes in otherwise healthy patients. Careful monitoring and cautious application of this technique in patients with pre-existing cardiopulmonary disorders will be required to prevent acute decompensation.

Acidosis, Respiratory↗
PubMed1996

Comparative stress hormone changes during helium versus carbon dioxide laparoscopic cholecystectomy.

Laparoscopic surgery has been termed minimally invasive surgery by advocates of this technology. It has been demonstrated previously that using carbon dioxide for insufflation produces a respiratory acidosis due to transperitoneal absorption of gas. Insufflation with helium does not create this acidosis. We questioned whether laparoscopic surgery would elicit a stress response and whether the absence of acidosis with helium might prevent or reduce the levels of stress hormones. Sixteen female patients undergoing laparoscopic cholecystectomy were randomly assigned to helium (n = 8) or CO2 (n = 8) insufflation. Serum cortisol, epinephrine, and norepinephrine were measured preoperatively, after induction of anesthesia but before insufflation, at 45 min of surgery, and after desufflation. There were increases in epinephrine, norepinephrine, plasma cortisol, and urine cortisol at 45 min and at the conclusion of the procedure over the preoperative value. With ANOVA, each variable showed significant increases from preoperative values, at 45 min, and at the end of the case. Except for the increased epinephrine when helium was used, there were no significant differences in the other variables between helium and CO2. Laparoscopic cholecystectomy produces significant increases in stress hormone levels. Prevention of acidosis with helium insufflation does not appear to protect against increases in stress hormones. Epinephrine levels with helium insufflation are higher than with CO2, and elevations in stress hormones suggest that laparoscopic cholecystectomy is not physiologically minimally invasive.

Acidosis, Respiratory↗
PubMed2006

Nerve excitability changes in critical illness polyneuropathy.

Patients in intensive care units frequently suffer muscle weakness and atrophy due to critical illness polyneuropathy (CIP), an axonal neuropathy associated with systemic inflammatory response syndrome and multiple organ failure. CIP is a frequent and serious complication of intensive care that delays weaning from mechanical ventilation and increases mortality. The pathogenesis of CIP is not well understood and no specific therapy is available. The aim of this project was to use nerve excitability testing to investigate the changes in axonal membrane properties occurring in CIP. Ten patients (aged 37-76 years; 7 males, 3 females) were studied with electrophysiologically proven CIP. The median nerve was stimulated at the wrist and compound action potentials were recorded from abductor pollicis brevis muscle. Strength-duration time constant, threshold electrotonus, current-threshold relationship and recovery cycle (refractoriness, superexcitability and late subexcitability) were recorded using a recently described protocol. In eight patients a follow-up investigation was performed. All patients underwent clinical examination and laboratory investigations. Compared with age-matched normal controls (20 subjects; aged 38-79 years; 7 males, 13 females), CIP patients exhibited reduced superexcitability at 7 ms, from -22.3 +/- 1.6% to -7.6 +/- 3.1% (mean +/- SE, P approximately 0.0001) and increased accommodation to depolarizing (P < 0.01) and hyperpolarizing currents (P < 0.01), indicating membrane depolarization. Superexcitability was reduced both in patients with renal failure and without renal failure. In the former, superexcitability correlated with serum potassium (R = 0.88), and late subexcitability was also reduced (as also occurs owing to hyperkalaemia in patients with chronic renal failure). In patients without renal failure, late subexcitability was normal, and the signs of membrane depolarization correlated with raised serum bicarbonate and base excess, indicating compensated respiratory acidosis. It is inferred that motor axons in these CIP patients are depolarized, in part because of raised extracellular potassium, and in part because of hypoperfusion. The chronic membrane depolarization may contribute to the development of neuropathy.

Acidosis, Respiratory↗
PubMed1999

Venous blood pressure in broilers during acute inhalation of five percent carbon dioxide or unilateral pulmonary artery occlusion.

We evaluated the hypothesis that venous congestion (increased venous volume), as reflected by venous hypertension (increased venous pressure), can arise when the right ventricle is unable to elevate the pulmonary arterial pressure sufficiently to propel the cardiac output through an anatomically inadequate or inappropriately constricted pulmonary vasculature. Changes in venous pressure were evaluated in clinically healthy broilers during modest increases in pulmonary vascular resistance induced by inhalation of 5% CO2 and during large increases in pulmonary vascular resistance accomplished by acutely tightening a snare around one pulmonary artery. Inhalation of 5% CO2 induced a pronounced respiratory acidosis, as reflected by increases the partial pressure of CO2 and the hydrogen ion concentration in arterial blood. Inhalation of 5% CO2 also increased pulmonary arterial pressure by approximately 3 mm Hg and increased venous pressure by approximately 1 mm Hg when compared with the pre-inhalation venous pressure. Tightening the pulmonary artery snare increased the pulmonary arterial pressure by approximately 10 mm Hg, and this degree of pulmonary hypertension was sustained until the snare was released. When compared with the pre- and post-snare intervals, tightening of the pulmonary artery snare induced a sustained increase in venous pressure of > or = 1 mm Hg. Veins have highly compliant walls that permit an approximate doubling in volume with only small (4 to 6 mm Hg) increases in central venous pressure. Presumably the apparently modest 1 mm Hg increase in venous pressure measured after CO2 inhalation or unilateral pulmonary artery occlusion reflects a large increase in venous volume and, thus, substantial venous congestion. These observations support the hypothesis that increases in pulmonary vascular resistance can initiate increases in venous pressure by challenging the capacity of the right ventricle to propel all of the returning venous blood through the lungs. Central venous congestion predisposes broilers to the onset of cirrhosis and ascites by impeding the outflow of hepatic venous blood and increasing the hydrostatic pressure within hepatic sinusoids.

Acidosis, Respiratory↗
PubMed1996

Tracheal extubation of children in the operating room after atrial septal defect repair as part of a clinical practice guideline.

Early tracheal extubation in the operating room after atrial septal defect (ASD) surgery was recommended as part of a clinical practice guideline (CPG) established in the Cardiovascular Program at the Children's Hospital, Boston, MA. This retrospective review was undertaken to determine whether this practice was efficient without compromising patient care. The charts and hospital charges for 102 patients undergoing secundum ASD or sinus venosus defect surgery between March 1992 and July 1994 were reviewed; 36 patients (Group I) had surgery prior to introduction of the CPG, and 66 patients were managed according to the CPG. Of the latter, 25 patients (Group II) were tracheally extubated in the operating room (OR) and 41 patients (Group III) were extubated in the cardiac intensive care unit (CICU). Patients in all three groups were similar with respect to height, weight, and surgical conditions including cardiopulmonary bypass time, lowest esophageal temperature, hematocrit, total OR time, and the time from completion of bypass to leaving the OR. Patients in Group II received significantly less fentanyl during anesthesia, were more likely to have a respiratory acidosis on admission to the CICU, and had an increased frequency of vomiting in the CICU. There was no difference in duration of CICU stay among groups. The length of hospital stay was reduced in Groups II and III after introduction of the CPGs, but was not influenced by tracheal extubation in the OR. There was no difference among groups in the hospital charges for OR, anesthesia and CICU time. However, when the combined hospital charges for services provided both in the OR and CICU were included, patients in Group II were charged significantly less, and this primarily reflects the absence of postoperative mechanical ventilation charges. Tracheal extubation in the OR after ASD surgery in children can result in lower patient charges without significantly compromising patient care.

Acidosis, Respiratory↗
PubMed1975

Cardiovascular responses to calcium administered intravenously to man during halothane anesthesia.

Calcium chloride (7 mg/kg) was administered intravenously to six healthy volunteers anesthetized with halothane. Cardiovascular changes were measured during constant ventilation and anesthetic depth under three conditions: 1) respiratory alkalosis, 2) normocarbia, and 3) respiratory acidosis. At each Paco2, calcium infusion significantly increased cardiac index, left ventricular minute work index, and stroke index. Heart rate, total peripheral resistance, and cardiac pre-ejection period decreased. No significant change in mean arterial blood pressure or central venous pressure followed calcium administration, and no arrhythmias occurred. It is concluded that calcium administration increases myocardial performance, presumably by increasing the availability of intracellular calcium ion for actomyosin interaction.

Acidosis, Respiratory↗
PubMed1986

Acute bronchospasm resembling status asthmaticus during the neonatal period.

Recently, we encountered four neonates who developed severe reversible partial lower airway obstruction. This communication describes their clinical course and the pathogenesis and treatment of acute bronchospasm resembling status asthmaticus and leading to life-threatening respiratory acidosis.

Acidosis, Respiratory↗
PubMed2000

Comparison of various hemoglobin polyoxyethylene conjugate solutions as resuscitative fluids after hemorrhagic shock.

BACKGROUND: Previous research suggested that splanchnic hypoperfusion occurs after resuscitation with certain acellular hemoglobin solutions. We examined the influence of maltose content and oxygen affinity on resuscitation with various hemoglobin polyoxyethylene conjugate solutions after hemorrhage. METHODS: Fifteen swine underwent hemorrhage and equal volume resuscitation with pyridoxalated hemoglobin polyoxyethylene conjugate containing 0% or 8% maltose, or low P50 conjugate, which also contained 8% maltose. Five control animals were monitored but not bled. Regional blood flow was determined by using radioactive microspheres, gastric mucosal perfusion was estimated with tonometry, and gut histopathology was evaluated. RESULTS: All hemoglobin solutions produced vasoconstriction, manifested by elevated mean systemic and pulmonary artery pressures without a significant decrease in cardiac index compared with the sham group. Resuscitation with maltose-containing solutions elevated arterial and regional PCO2 and depressed arterial pH and gastric pHi (p < 0.05 for all). Splanchnic and renal blood flows were reduced in the low P50 + 8% maltose group (p < 0.05 vs. sham and baseline for renal blood flow), possibly indicating greater regional vasoconstriction in this group. Ileal mucosal damage was more severe in the maltose-containing groups and correlated with decreased pHi. CONCLUSION: Vasoconstriction occurred in all groups but was more severe in the low P50 + 8% maltose group. Maltose-containing solutions caused respiratory acidosis, decreased pHi, and histologic evidence of mucosal injury. Pyridoxalated hemoglobin polyoxyethylene conjugate without maltose was a superior resuscitation solution in this swine model.

Acidosis, Respiratory↗
PubMed1986

Correlation of the one-minute Apgar score and umbilical cord acid-base status.

The one-minute Apgar score has proven useful by ensuring rapid assessment of the neonate, but is often poorly correlated with other indicators of intrauterine well-being. Since fetal asphyxia is directly associated with neonatal acidosis, a low Apgar score in the face of normal pH and base deficit does not indicate an asphyxiated infant. In a study to ascertain the feasibility of combining umbilical artery pH with the one-minute Apgar score for neonatal assessment, umbilical artery pH and Apgar scores were obtained on 212 singleton pregnancies. When the Apgar score was less than 7, more than half (60%) of the neonates had a normal umbilical artery pH. Fifty-one percent of this group had had intubation and nasopharyngeal suctioning, procedures known to be associated with lowered Apgar scores. When reviewing the umbilical artery gas values and base deficit in those neonates with a pH less than 7.20, we found that of the eight patients with an Apgar score of 7 or greater, seven (87.5%) were classified as having metabolic acidosis, with only one having respiratory acidosis. In the neonates with Apgar scores of less than 7, approximately two thirds had blood gas values compatible with metabolic acidosis, while the others displayed respiratory acidosis. We recommend, therefore, that neonates with a one-minute Apgar score less than 7 have umbilical artery pH determinations to confirm the presence or absence of acidosis. We also recommend that when the pH is less than 7.20, a complete set of gas values be evaluated with that specimen. This information offers more precise confirmation of the diagnosis of fetal distress and neonatal asphyxia, both for treatment and more reliable follow-up data, as well as for medicolegal purposes.

Acid-Base Equilibrium↗
PubMed2004

Pressure-controlled ventilation in children with severe status asthmaticus.

OBJECTIVE: The optimum strategy for mechanical ventilation in a child with status asthmaticus is not established. Volume-controlled ventilation continues to be the traditional approach in such children. Pressure-controlled ventilation may be theoretically more advantageous in allowing for more uniform ventilation. We describe our experience with pressure-controlled ventilation in children with severe respiratory failure from status asthmaticus. DESIGN: Retrospective review. SETTING: Pediatric intensive care unit in a university-affiliated children's hospital. PATIENTS: All patients who received mechanical ventilation for status asthmaticus. INTERVENTIONS: Pressure-controlled ventilation was used as the initial ventilatory strategy. The optimum pressure control, rate, and inspiratory and expiratory time were determined based on blood gas values, flow waveform, and exhaled tidal volume. MEASUREMENT AND MAIN RESULTS: Forty patients were admitted for 51 episodes of severe status asthmaticus requiring mechanical ventilation. Before the institution of pressure-controlled ventilation, median pH and Pco(2) were 7.21 (range, 6.65-7.39) and 65 torr (29-264 torr), respectively. Four hours after pressure-controlled ventilation, median pH increased to 7.31 (6.98-7.45, p <.005), and Pco(2) decreased to 41 torr (21-118 torr, p <.005). For patients with respiratory acidosis (Pco(2) >45 torr) within 1 hr of starting pressure-controlled ventilation, the median length of time until Pco(2) decreased to <45 torr was 5 hrs (1-51 hrs). Oxygen saturation was maintained >95% in all patients. Two patients had pneumomediastinum before pressure-controlled ventilation. One patient each developed pneumothorax and subcutaneous emphysema after initiation of pressure-controlled ventilation. All patients survived without any neurologic morbidity. Median duration of mechanical ventilation was 29 hrs (4-107 hrs), intensive care stay was 56 hrs (17-183 hrs), and hospitalization was 5 days (2-20 days). CONCLUSIONS: Based on this retrospective study, we suggest that pressure-controlled ventilation is an effective ventilatory strategy in severe status asthmaticus in children. Pressure-controlled ventilation represents a therapeutic option in the management of such children.

Acidosis, Respiratory↗
PubMed1994

Tracheal agenesis.

Agenesis of the trachea is a rare anomaly. The main signs are respiratory distress and cyanosis, inability to vocalize and impossible tracheal intubation. In most cases concomitant congenital anomalies of the heart, digestive tract or genitourinary tract are present. Endoscopy and X ray studies will confirm the diagnosis. There is no long-term surgical solution because no suitable material for a tracheal prosthesis is available at present, therefore the condition is ultimately fatal. We report a case of tracheal agenesis. After the diagnosis was established the baby's lungs were ventilated for several hours via an oesophageal tube and two broncho-oesophageal fistulae, but she finally died from untreatable respiratory acidosis. Autopsy revealed a Floyd's type III tracheal agenesis and a laryngeal cleft.

Acidosis, Respiratory↗