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PubMedDate not supplied

Effects of intravenous hyperosmotic sodium bicarbonate on arterial and cerebrospinal fluid acid-base status and cardiovascular function in calves with experimentally induced respiratory and strong ion acidosis.

The objectives of this study were to determine the effects of hyperosmotic sodium bicarbonate (HSB) administration on arterial and cerebrospinal fluid (CSF) acid-base balance and cardiovascular function in calves with experimentally induced respiratory and strong ion (metabolic) acidosis. Ten healthy male Holstein calves (30-47 kg body weight) were instrumented under halothane anesthesia to permit cardiovascular monitoring and collection of blood samples and CSE Respiratory acidosis was induced by allowing the calves to spontaneously ventilate, and strong ion acidosis was subsequently induced by i.v. administration of L-lactic acid. Calves were then randomly assigned to receive either HSB (8.4% NaHCO3; 5 ml/kg over 5 minutes, i.v.; n=5) or no treatment (controls, n=5) and monitored for 1 hour. Mixed respiratory and strong ion acidosis was accompanied by increased heart rate, cardiac index, mean arterial pressure, cardiac contractility (maximal rate of change of left ventricular pressure), and mean pulmonary artery pressure. Rapid administration of HSB immediately corrected the strong ion acidosis, transiently increased arterial partial pressure of carbon dioxide (P(CO2)), and expanded the plasma volume. The transient increase in arterial P(CO2) did not alter CSF P(CO2) or induce paradoxical CSF acidosis. Compared to untreated control calves, HSB-treated calves had higher cardiac index and contractility and a faster rate of left ventricular relaxation for 1 hour after treatment, indicating that HSB administration improved myocardial systolic function. We conclude that rapid i.v. administration of HSB provided an effective and safe method for treating strong ion acidosis in normovolemic halothane-anesthetized calves with experimentally induced respiratory and strong ion acidosis. Fear of inducing paradoxical CSF acidosis is not a valid reason for withholding HSB administration in calves with mixed respiratory and strong ion acidosis.

Acid-Base Equilibrium↗
PubMed1995

Intrapartum amniotic fluid index for predicting fetal acidemia. Results of receiver operating characteristic curve analysis.

OBJECTIVE: The objective of this study was to determine if the discriminatory intrapartum amniotic fluid index can reliably predict respiratory or metabolic acidosis in the newborn. STUDY DESIGN: Among 256 parturients at 37 weeks' gestation or more, the intrapartum amniotic fluid index was obtained in early labor, and umbilical arterial blood gas analysis was performed within 30 minutes of delivery. The mean (+/- SD) amniotic fluid indices in labor among newborns with no acidosis versus those with respiratory or metabolic acidosis were compared. A receiver operating characteristic curve was used to determine the best discriminatory intrapartum amniotic fluid index for respiratory and metabolic acidosis. RESULTS: Statistical analysis revealed that the mean intrapartum amniotic fluid index among 12 newborns with respiratory acidosis and 26 with metabolic acidosis was significantly lower than the mean index in 218 newborns without fetal acidemia. Despite the differences in the mean intrapartum amniotic fluid index in the three groups analyzed, the receiver operating characteristic curve indicated that an intrapartum amniotic fluid index alone is a poor test for predicting acidosis (respiratory or metabolic) in the neonate. CONCLUSION: The mean intrapartum amniotic fluid index in labor among newborns with respiratory or metabolic acidosis was significantly lower than that among nonacidotic newborns. The receiver operating characteristic curve indicated that the intrapartum amniotic fluid index cannot reliably distinguish nonacidotic infants from those with respiratory or metabolic acidosis.

Acidosis↗
PubMed1977

[Acidosis and clinical condition in asphyctic calves].

In depressed calves (modified APGAR score 4-6) there is at birth an evident combined respiratory-metabolic acidosis (pH = 7.082 +/- 0.175; pCO2 = 73.3 +/- 26.8 mm Hg; BE = -10.6 +/- 7.2 mmol/l). The metabolic adaptation is completed after 6 hours, the respiratory acidosis is present up to 24 hours after delivery. In comparison to normal calves there are significant deviations in pH-values, base excess standard bicarbonate and actual bicarbonate during the whole investigation time. The carbon dioxide tensions of the depressed calves are at birth similar to those of normal calves, but in the following hours they are significantly higher. A definite relationship can be demonstrated between the 1 minute APGAR score and pH-value, base excess, standard bicarbonate and actual bicarbonate. Oxygen tension, oxygen saturation and carbon dioxide do not correlate with the clinical condition.

Acidosis↗
PubMed1978

Interaction between PCO2 and plasma [HCO-3] in regulation of CSF [HCO-3] in respiratory alkalosis and metabolic acidosis.

The results of studies presented may be interpreted in light of the dual contribution theory of regulation of CSF acid-base balance, indicating significant interaction between systemic and local CNS mechanisms in H+ homeostasis in the brain and CSF. Both systemic and local mechanisms are at work in H+ homeostasis in the brain and CSF and depending on the specific acid-base disorder or the duration of the imbalance one or the other of the two factors may be the dominant one in maintaining H+ levels in the "normal" range. These factors come into play only when there has been a change in central pH with the primary aim of bringing the CNS [H+] towards normal.

Acidosis↗
PubMed1994

Newborn complications after intrapartum asphyxia with metabolic acidosis in the term fetus.

OBJECTIVES: Our purpose was to determine the newborn complications after respiratory or metabolic acidosis at delivery and to demonstrate the characteristics of an asphyxial insult predictive of these complications. STUDY DESIGN: Fifty-nine term fetuses with metabolic acidosis were matched with 59 fetuses with normal blood gas measures at delivery. Fifty-one fetuses with respiratory acidosis were also examined. A complication score expressed the magnitude of newborn complications during the 10 days after delivery. RESULTS: Newborn complications were not increased after respiratory acidosis. Newborn complications after metabolic acidosis increase in frequency and severity with the increasing severity and duration of the metabolic acidosis. Thirty-two of the 59 newborns in the metabolic acidosis group had a high complication score. The index values predictive of high scores were the duration of the metabolic acidosis and the Apgar score at 1 minute. CONCLUSIONS: Intrapartum fetal asphyxia with a severe metabolic acidosis accounts for complications in all newborn systems. The probability of a high complication score increases from 14% with favorable index values to 85% with unfavorable index values.

Acidosis↗
PubMed1980

[The influence of arterial partial pressure of co2 and of the arterial value of ph on endogenous catecholamines during extracorporal circulation in regard to oxygen consumption of the whole body (author's transl)].

Ten patients with coronary heart diseases were studied during total hypothermic extracorporal circulation relating changes of the endogenous catecholamines epinephrine and nor-epinephrine to arterial partial pressure of CO2 and to the arterial value of pH. Both of the catecholamines increased significantly during respiratory or metabolic acidosis whereas respiratory or metabolic alkalosis was accompanied by significantly lower catecholamine levels in blood. The changes in total peripheral resistance due to the endogenous blood levels of catecholamines depended proprotionally. Total peripheral resistance increased significantly due to increasing arterial level of both of the catecholamines. The results are discussed in consideration of oxygen consumption of the whole body during extracorporal circulation. It is known that the decrease of oxygen consumption of the whole body due to acidosis and due to an increased total peripheral resistance is accompanied by high catecholamine levels in blood. Increased hypothermic sympatho-adrenal activity during extracorporal circulation should not in any case cause in increase of oxygen consumption of the whole body.

Acidosis↗
PubMed1997

[Base excess] and [strong ion difference] during O2-CO2 exchange.

Detecting uptake or production of "metabolic acid" by a given tissue is often of interest. [Base excess] ([BE]) is the change in [strong acid] or [strong base] needed to restore pH to normal at normal PCO2. However, [BE] seems to have the potential for minor inaccuracy during hypercarbia, and venous blood is hypercarbic relative to arterial. Another approach is [strong ion difference] ([SID]), where a strong ion is one that is always dissociated in solution, and where [SID] = [strong cation] - [strong anion]. The hypothesis was tested that a-v [SID]p might be used to detect metabolic acid uptake or production by tissue. A computer simulation of O2-CO2 exchange was performed, using the Siggaard-Andersen [BE] equations, which provide an existing conceptual template. It was assumed that a change in [BE] = a change in [SID] (Adv. Exp. Med. Biol., in press). (A-v) [SID]p decreased linearly with decreasing [HbO2] during equimolar O2-CO2 exchange (delta mEq [SID]p.l-1 per delta gHbO2.dl-1 = 0.6, r2 = 1.0), and erythrocyte [BE] ([BE]e) and [SID]e decreased commensurately, such that [BE]WB remained constant. These changes represent ion exchanges between erythrocyte and plasma, governed by the Gibbs-Donnan equilibrium. It is concluded that a-v [SID]p may be used to examine a-v differences in [metabolic acid], based in [BE] concepts. The concentration of "metabolic acid" ([metabolic acid]) in blood increases during endotoxemia, exercise and shock. To identify organ(s) responsible, it is necessary to measure arteriovenous [strong acid]. Two methods are available. Whole blood base excess ([BE]WB), is the change in [strong acid]WB or [strong base]WB needed to restore plasma pH (pHp) to 7.4 at PCO2 of 40 torr, and is an excellent method for distinguishing "respiratory," from "metabolic" acidosis in arterial blood. However, while [BE] is most helpful conceptually, use of [BE] in venous blood presents two problems. First, [BE]WB may employ in vitro assumptions that are slightly inaccurate during hypercarbia in vivo, and venous blood is hypercarbic relative to arterial. The problem seems to be that [BE] assumes greater [hemoglobin] ([Hb]) than is actually effective in vivo, where Hb is diluted in the extracellular volume. The "Van Slyke" version of the [BE]WB equation is: BE]WB = ¿[HCO3-]p - 24.4 + (2.3 x [Hb] + 7.7) x (pHp - 7.4)¿ x (1-0.023 x [Hb]) (1) This equation may be thought of conceptually as: [BE] = ([HCO3-] + [A-]) - (normal [HCO3-] + normal [A-]) (2) where A- is negatively charged non-volatile weak acid. Missing or excess charges are attributed to abnormal [strong acid] or [strong base], and [A-]WB is computed using actual, as opposed to effective, [Hb]. This problem has been adequately addressed in arterial blood by standard [BE]WB ([SBE]WB), by assuming that effective [Hb] in vivo is approximately one third of that in vitro. However, it is not clear whether this assumption is sufficiently accurate to examine arteriovenous differences. A second and related problem with using [BE] to detect (a-v) differences is the magnitude of change in Hb buffering in vivo during O2 desaturation. Desaturation renders Hb a stronger weak acid buffer, i.e. increases its effective pK value. Consequently, [HCO3-]p is greater at any given PCO2, creating the appearance of a larger [BE]WB, whereas [strong acid] or [strong base] has not changed. This artifact can be corrected using the "O2 desaturation transform factor," which is 0.19 mM delta g [HbO2].dl-1 in vitro. In vivo, however, the magnitude of the O2 desaturation transform factor might be different. An alternative approach to acid-base analysis is strong ion difference (SID) where a strong ion is one that is always dissociated in physiologic solution. [SID] can usually be approximated as: [Na+] + [K+] - [Cl-] - [La-]. Although [BE] does not equal [SID], a change in [BE] must always accompany a change in [SID], and vice-versa. While the [SID] approach is tedious, and often unnecessarily so, [SID] ca

Acid-Base Equilibrium↗
PubMed1991

The syndrome of alcoholic ketoacidosis.

PURPOSE: To further elucidate the clinical spectrum of alcoholic ketoacidosis (AKA). PATIENTS AND METHODS: A case series of 74 patients with AKA defined as a wide anion gap metabolic acidosis unexplained by any other disorder or toxin, including any patient with a history of chronic alcohol abuse. The setting was the Medical Emergency Department at Grady Memorial Hospital in Atlanta, Georgia, a university-affiliated inner-city hospital. RESULTS: AKA is a common disorder in the emergency department, more common than previously thought. The acid-base abnormalities are more diverse than just a wide-gap metabolic acidosis and often include a concomitant metabolic alkalosis, hyperchloremic acidosis, or respiratory alkalosis. Lactic acidosis is also common. Semiquantitative serum acetoacetate levels were positive in 96% of patients. Elevated blood alcohol levels were present in two thirds of patients in whom alcohol levels were determined, and levels consistent with intoxication were seen in 40% of these patients. Electrolyte disorders including hyponatremia, hypokalemia, hypophosphatemia, hyperglycemia, hypocalcemia, and hypomagnesemia were common on presentation. The most common symptoms were nausea, vomiting, and abdominal pain. The most common physical findings were tachycardia, tachypnea, and abdominal tenderness. Altered mental status, fever, hypothermia, or other abnormal findings were uncommon and reflected other underlying processes. CONCLUSIONS: AKA is a common disorder in chronic malnourished alcoholic persons. The acid-base abnormalities reflect not only the ketoacidosis, but also associated extracellular fluid volume depletion, alcohol withdrawal, pain, sepsis, or severe liver disease. Although the pathophysiology is complex, the syndrome is rapidly reversible and has a low mortality.

Acid-Base Imbalance↗
PubMed1976

Congenital posterolateral diaphragmatic hernia.

The infant who is born with a posterolateral diaphragmatic hernia who becomes symptomatic at or soon after birth requires urgent care. Surgical reduction of the diaphragmatic hernia must be accomplished quickly. Respiratory and metabolic acidosis must be treated appropriately. The parents should be informed of the gravity of their infant's problem and reassurred by appropriate explanation of the nature of the defect and the therapeutic requirements. If the infant dies, the parents are in need of empathy, reassurance, and adequate explanation so that they do not have lingering doubts regarding the etiology of the anomaly and the adequacy of the therapy. If the infant lives, the medical team can share the feeling of a job well done.

Acidosis↗