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PubMed1997

The limitations of decision trees and automatic learning in real world medical decision making.

The decision tree approach is one of the most common approaches in automatic learning and decision making. The automatic learning of decision trees and their use usually show very good results in various "theoretical" environments. But in real life it is often impossible to find the desired number of representative training objects for various reasons. The lack of possibilities to measure attribute values, high cost and complexity of such measurements, and unavailability of all attributes at the same time are the typical representatives. For this reason we decided to use the decision trees not for their primary task--the decision making--but for outlining the most important attributes. This was possible by using a well-known property of the decision trees--their knowledge representation, which can be easily understood by humans. In a delicate field of medical decision making, we cannot allow ourselves to make any inaccurate decisions and the "tips," provided by the decision trees, can be of a great assistance. Our main interest was to discover a predisposition to two forms of acidosis: the metabolic acidosis and respiratory acidosis, which can both have serious effects on child's health. We decided to construct different decision trees from a set of training objects. Instead of using a test set for evaluation of a decision tree, we asked medical experts to take a closer look at the generated trees. They examined and evaluated the decision trees branch by branch. Their comments show that trees generated from the available training set mainly have surprisingly good branches, but on the other hand, for some, no medical explanation could be found.

Acidosis↗

PubMed1989

Brain pH responses to sodium bicarbonate and Carbicarb during systemic acidosis.

Rats subjected to ammonium chloride-induced metabolic acidosis or respiratory acidosis caused by hypercapnia were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride induced dose-dependent systemic acidosis but did not affect intracellular brain pH. Hypercapnia caused dose-dependent systemic acidosis as well as decreases in intracellular brain pH. Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial PCO2 in both acidosis models, but it caused intracellular brain acidification in rats with ammonium chloride acidosis. Carbicarb therapy resulted in systemic alkalinization without major changes in arterial PCO2 and intracellular brain alkalinization in both acidosis models. These data demonstrate that bicarbonate therapy of systemic acidosis may be associated with "paradoxical" intracellular brain acidosis, whereas Carbicarb causes both systemic and intracellular alkalinization under conditions of fixed ventilation.

Acidosis↗

PubMed2003

[Acute encephalopathy due to thiamine deficiency with hyperammonemia in a chronic hemodialysis patient: a case report].

Hemodialysis(HD) patients are at risk for thiamine deficiency because of low intake and accelerated loss of thiamine during HD. We report here an HD patient, an 82-year-old woman, who developed acute encephalopathy due to thiamine deficiency with hyperammonemia. She was admitted to Nishikawa Town Hospital due to pneumonia and was treated with ABPC/SBT for one week. While she was cured of pneumonia, she had a persistently poor appetite. On the twenty-fourth day after admission, HD with intradialytic parenteral nutrition(IDPN), which consisted of 10% glucose 500 ml, in order to correct her malnutrition, was started. She suddenly presented confusion, speech disturbance and ophthalmoplegia. HD with IDPN was stopped after two hours because of her symptoms. Laboratory studies disclosed plasma glucose of 186 mg/dl and serum ammonium of 155 micrograms/dl. Arterial blood gas analysis(inhaling 3 l/min O2) showed severe metabolic acidosis and respiratory acidosis (pH 7.138, pCO2 44.8 mmHg, pO2 108.9 mmHg, HCO3- 15.1 mmol/l). Her malnutrition, unexplained metabolic acidosis and neurological presentation raised the suspicion of acute encephalopathy due to thiamine deficiency. Fursultiamine 100 mg was administered intravenously. After two hours, metabolic acidosis disappeared (pH 7.437, pCO2 33.9 mmHg, pO2 161.0 mmHg, HCO3- 22.9 mmol/l), and she regained her clear consciousness and serum ammonium decreased at 16 micrograms/dl on the next morning. Serum lactate and thiamine level were shown later to be 57.5 mg/dl and 27 nmol/l, respectively. Her clinical course suggests that the glucose load including IDPN may have caused deterioration of the neurological disorder under the condition of thiamine deficiency. Furthermore, it is possible that a relationship exists between thiamine deficiency and hyperammonemia.

Acidosis, Lactic↗

PubMed1992

[Metabolic acidosis in severe acute asthma. Effect of alkaline therapy].

Respiratory acidosis of severe acute asthma is a severity factor. In this paper the treatment of associated metabolic acidosis is discussed. Among 34 consecutive episodes of severe acute asthma with acidosis (pH < 7.35) treated with continuous adrenaline perfusion, theophylline and hydrocortisone hemisuccinate, respiratory acidosis was observed in 12, metabolic acidosis in 2 and mixed respiratory and metabolic acidosis in 20. The association of hypercapnic acidosis with hypochloraemic acidosis reflected a time of installation longer than when respiratory acidosis only was present (p < 0.05). Among the 22 patients who had metabolic acidosis on admission, 14 were treated with 168 +/- 82 mmol of sodium bicarbonate, the remaining 8 patients being untreated and acting as controls. The rapidity with which pH was corrected was the same in the treated and untreated groups (9.1 +/- 5.5 hours vs 6.7 +/- 3.7 hours), whereas dyspnoea (respiratory rate < 18/min) was more rapidly corrected in the treated group that in controls (11.6 +/- 5.7 hours vs 5.9 +/- 5.9 hours; p < 0.05). It is concluded that in more than 50% of the cases respiratory acidosis of severe acute asthma is associated with a metabolic acidosis. Correcting this metabolic acidosis with sodium bicarbonate results in improvement of respiration, perhaps by facilitating the action of bronchodilator catecholamines.

Acidosis↗

PubMed1988

Acidemia alone does not stimulate rat renal Na+-H+ antiporter activity.

To examine whether systemic acidemia is the cause of the adaptive increase in renal brush-border membrane (BBM) Na+-H+ exchange activity seen in metabolic acidosis, we examined the time course of changes in Na+-H+ exchange activity in rats with chronic metabolic or respiratory acidosis. Metabolic acidosis was created by allowing rats free access to a 1.5% NH4Cl drinking solution. Respiratory acidosis was created by housing rats in a chamber designed to maintain ambient PCO2 levels at 10%. All rats were fed normal rat chow. Control and respiratory acidosis rats had free access to tap water. Rats from each group were studied 1, 3, 5, 7, and 14 days after onset of treatment. Na+-H+ exchange activity was examined in renal BBM vesicles using acridine orange. In both metabolic acidosis and respiratory acidosis, arterial blood [H+] increased markedly at day 1 and returned toward normal thereafter; at day 14, [H+] was elevated to a comparable degree in both groups. In metabolic acidosis, Na+-H+ exchange activity remained at control levels for 3 days but increased markedly thereafter. In contrast, in respiratory acidosis no adaptive increase in activity occurred at any time. Because no correlation was found between blood [H+] and renal BBM Na+-H+ exchange activity, we conclude that stimuli other than systemic acidemia are responsible for the adaptation seen in chronic metabolic acidosis.

Acidosis↗

PubMed2004

Melatonin attenuates rat carotid chemoreceptor response to hypercapnic acidosis.

Respiratory activity is under circadian modulation and the physiological mechanisms may involve the pineal secretory product, melatonin, and the carotid chemoreceptor. We hypothesized that melatonin modulates the carotid chemoreceptor response to hypercapnic acidosis. To determine whether the effect of melatonin on the chemoreceptor response to hypercapnic acidosis is mediated by melatonin receptors in the chemosensitive cells, cytosolic calcium ([Ca2+]i) was measured by spectrofluorometry in fura-2-loaded glomus cells dissociated from rat carotid bodies. Melatonin (0.01-10 nm) per se did not change the [Ca2+]i levels of the glomus cells but it concentration-dependently attenuated the peak [Ca2+]i response to hypercapnic acidosis in the glomus cells. In addition, the [Ca2+]i response was attenuated by 2-iodomelatonin, an agonist of melatonin receptors. The melatonin-induced attenuation of the [Ca2+]i response to hypercapnic acidosis was abolished by pretreatment with an non-selective mt1/MT2 antagonist, luzindole, and by MT2 antagonists, 4-phenyl-2-propionamidotetraline or DH97. In situ hybridization study with antisense mt1 and MT2 receptor mRNA oligonucleotide probes showed an expression of mt1 and MT2 receptors in the rat carotid body. Also, melatonin attenuated the carotid afferent response to hypercapnic acidosis in single- or pauci-fibers recorded from the sinus nerve in isolated carotid bodies superfused with bicarbonate-buffer saline. Results suggest that an activation of the melatonin receptors expressed in the glomus cells of the rat carotid body reduces the chemoreceptor response to hypercapnic acidosis. This modulation may play a physiological role in the influence of the circadian rhythms on the chemoreflex.

Acidosis, Respiratory↗

PubMed1981

Effects of acid-base changes on excitation--contraction coupling in guinea-pig and rabbit cardiac ventricular muscle.

1. Respiratory and metabolic acid-base changes caused similar steady-state changes in the contractility of cardiac ventricular muscle, but the rate of response was more rapid with the former intervention. 2. Variations in extracellular pCO2 and [HCO3-] at constant pH caused only a transient change in contractility. 3. An intracellular pH change can describe the above events. 4. The changes in contractility caused by extracellular acid-base changes could be explained by competition between Ca2+ and H+ ions for a single process. 5. Assuming an electroneutral scheme whereby one extracellular Ca2+ ion or two intracellular H+ ions compete for a binding site, the interior of ventricular cells must be better buffered than the extracellular fluid. 6. H+ ions evoked a release of Ca2+ ions from a mitochondrial suspension with a time course similar to the partial recovery of tension observed during a respiratory acidosis. 7. Respiratory and metabolic acidosis depressed the action potential plateau and prolonged repolarization. 8. The resting potential and the maximum rate of depolarization were unaffected by the above acid-base changes. 9. An acidosis depressed Ca2+ influx through the slow inward channel by an amount sufficient to account for the observed contractility changes. 10. It is concluded that between pH 7.6 and 6.6 the major physiological effect of an acidosis is to depress the slow inward current as a result of an intracellular pH change.

Acid-Base Equilibrium↗

PubMed1975

Intracellular pH and K+ of cardiac and skeletal muscle in acidosis and alkalosis.

The effects of a metabolic and respiratory acidosis and alkalosis on intracellular pH (pHi) and K+ have been compared in cardiac and skeletal muscle from the anesthetized rabbit. The extracellular space and pHi were calculated from the distribution volumes of [51Cr] EDTA and [14C]DMO, respectively. When pHe was varied by altering PCO2, the slope of the line relating pHi to the extracellular pH (pHe) was greater (P less than 0.05--0.001) than that obtained during metabolic changes of pHe in right and left ventricles, atria, diaphragm, and quadriceps. During metabolic acidosis and alkalosis, the slope of pHi/pHe line did not vary between tissues. During respiratory acidosis, there was no difference in slope between cardiac tissues, but it was less in left ventricle than quadriceps (P less than 0.001). In left ventricle intracellular K+ increased in a metabolic (P less than 0.05) or respiratory acidosis (P less than 0.02), whereas in diaphragm it decreased (P less than 0.02). Intracellular K+ correlated with pHe and pHE-PHi. Changes in pHi but not intracellular K+ could explain known differences in myocardial function in respiratory and metabolic acidosis.

Acidosis↗

PubMed1987

Renal ammoniagenesis following glutamine loading in intact dogs during acute metabolic acid-base perturbations.

Adaptation of renal ammoniagenesis during acute metabolic acidosis in intact dogs may be nonexistent or, at least, markedly less than in chronic acidosis. This contrasts to adaptation in acute respiratory acidosis, where levels similar to those attained in chronic acidosis occur within hours. Accordingly, the inability to discern marked changes in acute metabolic acidosis compared with acute respiratory acidosis has been attributed to decreased glomerular filtration rate and renal blood flow seen frequently in the former. In our studies, we found early changes in ammoniagenesis and glutamine metabolism during acute metabolic acidosis, but not of the magnitude seen in chronic acidosis, even considering the changes in renal blood flow (RBF) and glomerular filtration rate (GFR). Exogenous glutamine loading allowed us to discover that the qualitative changes in glutamine metabolism during acute metabolic acidosis differed from control but fell short of those seen in chronic metabolic a acidosis. We also examined glutamine metabolism when renal ammoniagenic adaptation was acutely inhibited in chronically acidotic dogs. Infusing NaHCO3 into chronically acidotic dogs decreased renal ammonia production significantly (247 mumol min-1 100 ml-1 GFR vs 148 mumol min-1 100 ml-1 GFR: P less than 0.001) and glutamine extraction (111.8 mumol min-1 100 ml-1 GFR vs 90.9 mumol min-1 100 ml-1 GFR: P less than 0.02). The qualitative changes in renal glutamine metabolism in both studies suggest that alterations in deamination of glutamate formed from glutamine are responsible, at least in part, for adaptation to acute acid-base perturbations. Compared with respiratory acidosis, adaptation to metabolic acidosis is progressive and prolonged.

Acid-Base Imbalance↗

PubMed1982

Acid-base imbalance and ulceration in the cold restrained rat.

Using the cold restrained rat model of stress ulceration, we have examined the influence of metabolic acidosis, metabolic alkalosis, and respiratory acidosis on the development of gastric erosions. The rats were restrained in tightly fitting perspex chambers at 6 degrees C for 3 hours. Acid-base imbalance was achieved by infusion of NH4Cl or NaHCO3 or by exposure to 5% CO2. The degree of ulceration was expressed by a lesion score of 0 to 4. The control group showed a score of 2.5 +/- 0.2 (mean +/- SEM). With metabolic acidosis the score was 3.6 +/- 0.2, and with metabolic alkalosis the score was 0.9 +/- 0.4. Both values were significantly different from control values (P less than 0.005). Respiratory acidosis was associated with a score similar to that of the control group. The values obtained appeared to be independent of gastric luminal acidity. The findings indicate that the systemic HCO-3 concentration is a significant determinant of the degree of ulceration in the cold restrained rat.

Acid-Base Imbalance↗

PubMed1987

Effects of acute acid-base changes on rat renal pyruvate dehydrogenase. Renal pyruvate dehydrogenase during acid-base alterations.

Glutamine, the principal source of urinary ammonia, can be fully oxidized or converted to glucose by the kidney. To be oxidized, the carbon skeleton of glutamine must enter the TCA cycle as acetyl CoA formed by pyruvate dehydrogenase (PDH). The purpose of this study was to measure kidney PDH activity (active and total) following acute acid-base changes in vivo. PDHa activity was elevated after acute metabolic alkalosis and acidosis and unchanged by respiratory acidosis. Kidney ADP/ATP, CoA/acetyl CoA and calculated mitochondrial NAD+/NADH ratios were also determined and revealed an increase in kidney ADP/ATP with alkalosis but no changes during metabolic and respiratory acidosis.

Acid-Base Imbalance↗

PubMed1987

Renal excretion of divalent ions in response to chronic acidosis: evidence that systemic pH is not the controlling variable.

Although metabolic acidosis produces calciuric, phosphaturic, and magnesiuric effects, the consequences of chronic respiratory acidosis are unclear. To examine the role of systemic pH on renal divalent metabolism, 4-day balance studies were performed in rats with both metabolic acidosis induced by adding 1.5% NH4Cl to the drinking water, and respiratory acidosis produced by exposure to 10% atmospheric CO2 in an environmental chamber, and in controls pair-fed with each group. By the fourth day, blood pH had decreased to an identical degree with both chronic metabolic and respiratory acidosis and averaged 7.28. As anticipated, chronic metabolic acidosis resulted in significant calciuria, magnesiuria, and phosphaturia. However, despite the similar decrement in blood pH, calcium, phosphorus, and magnesium excretion was similar to that in the pair-fed controls with chronic respiratory acidosis. These findings indicate that a low systemic pH, per se, does not account for the modifications in urinary divalent ion handling that accompany chronic metabolic acidosis. However, additional observations suggest that differences in the intracellular pH of the proximal tubular epithelium may be an important regulatory variable.

Acidosis↗

PubMed1980

Stimulation of ammoniagenesis by acute acidosis: evidence for a urinary inhibitor.

To elucidate the factors mediating the response of renal ammoniagenesis to acute acidosis, the isolated perfused rat kidney was subjected to acute metabolic and respiratory acidosis with either standard collection or drainage of urine back into the perfusate. Midway during a 90-min perfusion with 0.4 mM glutamine and 5 mM glucose, perfusate pH was decreased to 6.8 by addition of HCl or alteration of the PCO2. Metabolic acidosis increased NH3 production, acidified the urine, and increased urinary NH4 excretion. Respiratory acidosis increased NH3 production to a comparable degree without urine acidification and with a minimal increase in NH4 excretion. When respiratory acidosis preceded perfusion at control PCO2 levels, NH3 production was increased but NH4 excretion was lower than control values. If urine drained back into the perfusate, NH3 production was not altered by either metabolic or respiratory acidosis. Accordingly, acute changes in perfusate pH stimulate renal ammoniagenesis by the isolated perfusate pH stimulate renal ammoniagenesis by the isolated perfused kidney independent of changes in urinary pH and NH4 excretion. This response is inhibited by an unidentified factor excreted in the urine.

Acid-Base Equilibrium↗

PubMed1994

Acute acid-base disorders associated with status epilepticus.

OBJECTIVE: To analyze the acid-base abnormalities in patients with status epilepticus. DESIGN: We retrospectively reviewed the acid-base disturbances in 38 consecutive patients who had been admitted to the emergency department at a Mayo-affiliated hospital because of status epilepticus between 1982 and 1993. MATERIAL AND METHODS: On the basis of results of arterial blood gas analyses, the acid-base disorders were categorized. In addition, chest roentgenograms and electrocardiograms were reviewed for pulmonary infiltrates and cardiac arrhythmias. RESULTS: Arterial blood gas analysis performed immediately after admission revealed an acid-base abnormality in 32 of 38 patients (84%). Respiratory acidosis was most common (N = 16; 42%) and occurred either alone or in combination with metabolic acidosis. Pulmonary infiltrates were not more common in patients with respiratory acidosis than in other patients. Although cardiac arrhythmias were more common in patients with respiratory or metabolic acidosis (42%) than in those with respiratory alkalosis or normal blood gas values (36%), this difference was not statistically significant. CONCLUSION: We conclude that respiratory acidosis with or without metabolic acidosis is common in patients who have status epilepticus. Respiratory acidosis was not predictive of the final outcome. In our study patients, all acid-base abnormalities resolved spontaneously.

Acid-Base Imbalance↗

PubMed1999

Clinical assessment of acid-base status. Strong ion difference theory.

The traditional approach to evaluating acid-base balance uses the Henderson-Hasselbalch equation to categorize four primary acid-base disturbances: respiratory acidosis (increased PCO2), respiratory alkalosis (decreased PCO2), metabolic acidosis (decreased extracellular base excess), or metabolic alkalosis (increased extracellular base excess). The anion gap is calculated to detect the presence of unidentified anions in plasma. This approach works well clinically and is recommended for use whenever serum total protein, albumin, and phosphate concentrations are approximately normal; however, when their concentrations are markedly abnormal, the Henderson-Hasselbalch equation frequently provides erroneous conclusions as to the cause of an acid-base disturbance. Moreover, the Henderson-Hasselbalch approach is more descriptive than mechanistic. The new approach to evaluating acid-base balance uses the simplified strong ion model to categorize eight primary acid-base disturbances: respiratory acidosis (increased PCO2), respiratory alkalosis (decreased PCO2), strong ion acidosis (decreased [SID+]) or strong ion alkalosis (increased [SID+]), nonvolatile buffer ion acidosis (increased [ATOT]) or nonvolatile buffer ion alkalosis (decreased [ATOT]), and temperature acidosis (increased body temperature) or temperature alkalosis (decreased body temperature). The strong ion gap is calculated to detect the presence of unidentified anions in plasma. This simplified strong ion approach works well clinically and is recommended for use whenever serum total protein, albumin, and phosphate concentrations are markedly abnormal. The simplified strong ion approach is mechanistic and is therefore well suited for describing the cause of any acid-base disturbance. The new approach should therefore be valuable in a clinical setting and in research studies investigating acid-base balance. The presence of unmeasured strong ions in plasma or serum (such as lactate, ketoacids, and uremic anions) is best detected by calculating the SIG. The AG, actual bicarbonate concentration, and standard bicarbonate concentration all ignore the effects that changes in plasma protein and phosphate concentration have on plasma pH, thereby inevitably leading to inaccuracies in estimating the unmeasured strong ion concentration in plasma.

Acid-Base Equilibrium↗

PubMed2000

Clinical assessment of acid-base status: comparison of the Henderson-Hasselbalch and strong ion approaches.

The traditional approach for clinically assessing acid-base status uses the Henderson-Hasselbalch equation to categorize 4 primary acid-base disturbances: respiratory acidosis (increased PCO2), respiratory alkalosis (decreased PCO2), metabolic acidosis (decreased extracellular base excess or actual HCO3- concentration), and metabolic alkalosis (increased extracellular base excess or actual HCO3- concentration). The anion gap is calculated to detect unidentified anions in plasma. This approach works well clinically and is recommended for use whenever serum total protein, albumin, and phosphate concentrations are approximately normal. However, because the Henderson-Hasselbalch approach is more descriptive than mechanistic, when these concentrations are markedly abnormal the Henderson-Hasselbalch equation frequently provides erroneous information as to the cause of an acid-base disturbance. The new quantitive physicochemical approach to evaluating acid-base balance uses the simplified strong ion model to categorize 6 primary acid-base disturbances: respiratory acidosis (increased PCO2), respiratory alkalosis (decreased PCO2), strong ion acidosis (decreased strong ion difference), strong ion alkalosis (increased strong ion difference), nonvolatile buffer ion acidosis (increased plasma concentrations of albumin, globulins, or phosphate), and nonvolatile buffer ion alkalosis (decreased plasma concentrations of albumin, globulins, or phosphate). The strong ion gap is calculated to detect unidentified anions in plasma. The simplified strong ion approach works well clinically and is recommended for use whenever serum total protein, albumin, or phosphate concentrations are markedly abnormal. The simplified strong ion approach is mechanistic and is therefore well suited for describing the cause of any acid-base disturbance.

Journal Article↗

PubMed1988

Regulation of Na/H exchange in renal microvillus vesicles in chronic hypercapnia.

Several disturbances of acid-base balance, including chronic metabolic and respiratory acidoses and metabolic alkalosis, are associated with enhanced proximal tubule bicarbonate reabsorption. To determine whether augmented brush border Na/H exchange might mediate enhanced proximal tubule bicarbonate reabsorption in these disorders, we measured Na/H exchange activity in cortical brush border membrane vesicles (BBMV) prepared from rats and rabbits adapted to hypercapnia and other chronic acid-base disturbances. BBMV prepared from control animals and animals with chronic acid-base disturbances were similar as judged by marker enzymes, alkaline phosphatase, and ouabain-sensitive phosphatase. Despite profound respiratory acidosis, no increase in Na/H exchange activity could be detected in vesicles prepared from rats adapted to chronic (8 to 10 days) or subacute (24 hr) respiratory acidosis. In addition, vesicles prepared from rabbits exposed to chronic hypercapnia did not show increased Na/H exchange when compared with contemporaneous controls. By contrast, in agreement with previously published results, amiloride-sensitive sodium uptake was increased by 30% in vesicles derived from animals with ammonium chloride-induced acidosis compared with contemporaneous controls. Two models of chronic metabolic alkalosis were also studied; vesicles from alkalotic rats did not show any alteration in Na/H exchange. We conclude that metabolic acidosis, but not respiratory acidosis or metabolic alkalosis, leads to enhanced activity of the luminal Na/H exchanger.

Acid-Base Imbalance↗

PubMed1984

Effect of acidosis on bilirubin deposition in rat brain.

The effect of metabolic and respiratory acidosis on bilirubin and albumin entry into the brain was studied in 24 awake and unanesthetized rats. Hyperbilirubinemia was established by infusion of unconjugated bilirubin at a rate of 30 mg/kg/h for three hours. After two hours, metabolic acidosis was produced in eight rats by infusion of 0.5 N hydrochloric acid at a rate of 0.02 mL/g/h. This reduced the pH level to 7.03 +/- 0.01 (mean +/- SEM) with a normal value for PCO2. Respiratory acidosis was produced in another group of eight animals who breathed 20% CO2 in a balanced gas mixture for the last hour of the study period. This resulted in a reduction of pH to 7.04 +/- 0.01 with PCO2 of 100.4 +/- 2.3 mm Hg. A third group of eight rats served as controls and were given equal volumes of saline infusion. No increase in brain bilirubin or brain albumin was found in the group with metabolic acidosis, but in the group with respiratory acidosis both bilirubin and albumin concentrations in the brain increased significantly. No significant differences were found between the groups in serum total or apparent unbound bilirubin, albumin, or osmolality. The results indicate that a brief period of acidosis per se does not increase bilirubin entry into the brain, but hypercarbia does so by opening of the blood-brain barrier.

Acidosis↗