Respiratory Acid-base Disorders Research Articles

Alteration of Biochemical Parameters in Patients with Respiratory Acidosis and Alkalosis: A Hospital Based CrossSectional Study

Biochemical parameters like pH, pO2, pCO2, HCO3-, TCO2 and SO2 are frequently measured in critically ill patients with respiratory acidosis and alkalosis. These parameters have utmost importance in the assessment of ventilation, oxygenation and acid base status of these patients. The present study was undertaken to determine alteration of different biochemical parameters in patients with respiratory acidosis and alkalosis. This is a hospital based cross-sectional study conducted from May to December 2023, in the Department of Biochemistry, CMCTH. Arterial blood was collected and biochemical parameters like pH, pO2, pCO2, HCO3-, TCO2 and SO2 were measured using automated blood gas analyzer. Statistical analysis was done with SPSS version 21. This study showed that majority of the patients with respiratory acid-base disorder were females (58.1%) and elderly (41.8%). Respiratory acidosis and alkalosis were more common in elderly patients under age group 61- 70 years followed by >70 years category. Respiratory acidosis was accompanied by alteration of various ABG parameters like low pH, low pO2, high pCO2, high HCO3-, normal TCO2 and normal SO2 levels while respiratory alkalosis was accompanied by high pH, low pCO2, low HCO3-, low TCO2, normal sO2 and normal pO2 levels. Respiratory acid-base disorders are common in hospital settings with ailing respiratory diseases like COPD, Pneumonia, TB and Sepsis with higher incidences among elderly patients. Respiratory acidosis and alkalosis should be treated promptly giving highest consideration to various biochemical parameters in order to reduce comorbidities and mortalities associated with these conditions.

Cephalic and saphenous venous blood collected by continuous heating of the paws compared with arterial blood for measurement of blood gas values in well-perfused dogs.

"Arterialization" of the dorsal hand vein is well-established in human medicine, but not in veterinary medicine. To compare cephalic and saphenous venous blood collected by continuously heating the paws to 37°C ("arterialization"), with arterial blood (AB) for measurement of blood gas variables in well-perfused dogs. Eight healthy dogs. Experimental study. Fore and hind paws were continuously heated to 37°C to "arterialize" cephalic and saphenous venous blood. AB and "arterialized" cephalic and saphenous venous blood (ACV and ASV, respectively) were simultaneously collected from lightly anesthetized dogs with induced metabolic and respiratory acid-base disorders. The pH, partial pressures of carbon dioxide (PCO2 ) and oxygen (PO2 ), bicarbonate concentration [HCO3 - ], and base excess (BE) were measured once in each state. Systolic blood pressure was maintained above 100 mm Hg. The AB, ACV, and ASV values were compared. The pH, [HCO3 - ], and BE values had no significant difference and good agreement, the PCO2 values had a strong correlation (correlation coefficient of .91-1.00), and the PO2 values had a significant difference (P < .01) and poor agreement between AB and ACV, and between AB and ASV. The PCO2 values of ASV overestimated those of AB by ~3.0 mm Hg, which was considered within clinically allowable limits, while those of ACV were not within clinically allowable limits. Under experimental conditions, the ASV samples were more identical to the AB samples than the ACV samples for pH, PCO2 , [HCO3 - ], and BE values in well-perfused dogs. The saphenous vein is suitable for "arterialization."

Determinants of hypokalemia following hypertonic sodium bicarbonate infusion.

The hypokalemic response to alkali infusion has been attributed to the resulting extracellular fluid (ECF) expansion, urinary potassium excretion, and internal potassium shifts, but the dominant mechanism remains uncertain. Hypertonic NaHCO3 infusion (1 N, 5 mmol/kg) to unanesthetized dogs with normal acid-base status or one of the four chronic acid-base disorders decreased plasma potassium concentration ([K+]p) at 30 min in all study groups (Δ[K+]p, - 0.16 to - 0.73 mmol/L), which remained essentially unaltered up to 90-min postinfusion. ECF expansion accounted for only a small fraction of the decrease in ECF potassium content, (K+)e. Urinary potassium losses were large in normals and chronic respiratory acid-base disorders, limited in chronic metabolic alkalosis, and minimal in chronic metabolic acidosis, yet, ongoing kaliuresis did not impact the stability of [K+]p. All five groups experienced a reduction in (K+)e at 30-min postinfusion, Δ(K+)e remaining unchanged thereafter. Intracellular fluid (ICF) potassium content, (K+)i, decreased progressively postinfusion in all groups excluding chronic metabolic acidosis, in which a reduction in (K+)e was accompanied by an increase in (K+)i. We demonstrate that hypokalemia following hypertonic NaHCO3 infusion in intact animals with acidemia, alkalemia, or normal acid-base status and intact or depleted potassium stores is critically dependent on mechanisms of internal potassium balance and not ECF volume expansion or kaliuresis. We envision that the acute NaHCO3 infusion elicits immediate ionic shifts between ECF and ICF leading to hypokalemia. Thereafter, maintenance of a relatively stable, although depressed, [K+]e requires that cells release potassium to counterbalance ongoing urinary potassium losses.

Low noncarbonic buffer power amplifies acute respiratory acid-base disorders in patients with sepsis: an in vitro study.

Patients with sepsis have typically reduced concentrations of hemoglobin and albumin, the major components of noncarbonic buffer power (β). This could expose patients to high pH variations during acid-base disorders. The objective of this study is to compare, in vitro, noncarbonic β of patients with sepsis with that of healthy volunteers, and evaluate its distinct components. Whole blood and isolated plasma of 18 patients with sepsis and 18 controls were equilibrated with different CO2 mixtures. Blood gases, pH, and electrolytes were measured. Noncarbonic β and noncarbonic β due to variations in strong ion difference (βSID) were calculated for whole blood. Noncarbonic β and noncarbonic β normalized for albumin concentrations (βNORM) were calculated for isolated plasma. Representative values at pH = 7.40 were compared. Albumin proteoforms were evaluated via two-dimensional electrophoresis. Hemoglobin and albumin concentrations were significantly lower in patients with sepsis. Patients with sepsis had lower noncarbonic β both of whole blood (22.0 ± 1.9 vs. 31.6 ± 2.1 mmol/L, P < 0.01) and plasma (0.5 ± 1.0 vs. 3.7 ± 0.8 mmol/L, P < 0.01). Noncarbonic βSID was lower in patients (16.8 ± 1.9 vs. 24.4 ± 1.9 mmol/L, P < 0.01) and strongly correlated with hemoglobin concentration (r = 0.94, P < 0.01). Noncarbonic βNORM was lower in patients [0.01 (-0.01 to 0.04) vs. 0.08 (0.06-0.09) mmol/g, P < 0.01]. Patients with sepsis and controls showed different amounts of albumin proteoforms. Patients with sepsis are exposed to higher pH variations for any given change in CO2 due to lower concentrations of noncarbonic buffers and, possibly, an altered buffering function of albumin. In both patients with sepsis and healthy controls, electrolyte shifts are the major buffering mechanism during respiratory acid-base disorders.NEW & NOTEWORTHY Patients with sepsis are poorly protected against acute respiratory acid-base derangements due to a lower noncarbonic buffer power, which is caused both by a reduction in the major noncarbonic buffers, i.e. hemoglobin and albumin, and by a reduced buffering capacity of albumin. Electrolyte shifts from and to the red blood cells determining acute variations in strong ion difference are the major buffering mechanism during acute respiratory acid-base disorders.

Comparative Analysis of Acid-base Status Parameters in Newborn with Congenital Surgical Malformations During Perioperative Care Based on Types of Anesthesia

Introduction: Congenital malformations (CM) are most common in newborns and infants in the first year of life and require surgical correction in the first hours, days, months of life. Surgical interventions in severely ill babies with malformations can lead to catabolic stress, circulatory and respiratory disorders, metabolism shifts, water-electrolyte, protein, and acid-base status disorders.&#x0D; This study aimed to compare acid-base status in newborns and infants with congenital surgical pathology under different types of combined anesthesia. &#x0D; Materials and methods: This retrospective study included 150 newborns and infants with CM who required surgery. The patients were divided into three groups based on types of provided anesthesia: inhalation by Sevoran (sevoflurane) and regional anesthesia (group I); inhalation of Sevoran and intravenous anesthesia by Fentanyl (group II); and intravenous combination of Fentanyl and 20% Sodium Oxybutyrate (group III). The analysis included: acid-base status, peripheral oximetry, and the need for an oxygen mixture inhaled by the patient.&#x0D; Results In group I, there was a significant reduction in partial tension of CO2 and increased pH from the pre-surgical status, at the time of induction of anesthesia, during the most painful, traumatic stage, and after surgery compared to group II and III. Peripheral O2 saturation was not critically reduced at all stages of observation except in babies of group I compared to group III at the stage of induction of anesthesia (97.79 ± 2.45 vs. 98.79 ± 1.63, p = 0.0194) and at the most painful period of surgery (96.29 ± 3.47 vs. 98.10 ± 2.47, p = 0.0368). In group I, newborns and infants required higher oxygen concentrations in the inhalation mixture. There was a significant difference in FiO2 between groups I and III during the most painful stage of surgery (0.47 ± 0.29 and 0.33 ± 0.2, p = 0.0071), and immediately after surgery (0.34 ± 0, 19 and 0.26 ± 0.13, p = 0.0246).&#x0D; Conclusion: Among the newborns and infants with CM requiring surgical intervention and combined anesthesia, the most substantial acid-base status changes were observed in the group where anesthesia was provided by Sevoran (sevoflurane) and regional anesthesia (Group I).

Respiratory Acid-Base Disorders: Respiratory Acidosis and Respiratory Alkalosis

Respiratory acid-base disorders are divided into respiratory acidosis (which can be acute or chronic), and respiratory alkalosis (which also can be acute or chronic). The diagnosis is made after obtaining arterial blood gases (ABGs). Respiratory acidosis is also known as primary hypercapnia and is due to an increase in carbon dioxide (CO2) tension in bodily fluids. The metabolic compensation is an increase in serum bicarbonate (HCO3−), the increase is more pronounced in chronic respiratory acidosis. Oxygen administration (O2) is critical in the management of respiratory acidosis. Respiratory alkalosis or primary hypocapnia is due to a decrease in CO2 tension in bodily fluids. The metabolic compensation is a decrease in HCO3−, the decrease is more pronounced in chronic respiratory alkalosis. Rapid correction of respiratory alkalosis should be avoided, and the underlying etiology should be addressed.

Respiratory Acid-Base Disorders and Related Risk Factors in Critically Ill Patients

AbstractBackground: Respiratory acid-base disorders are commonly seen in the critical care setting and can occur independently or coexist with metabolic acid-base disorders. Aim of the study: To explore the pattern of respiratory acid-base disorders and related risk factors in critically ill patients. Design: the descriptive design was utilized in this study. Setting: This study was carried out in the Trauma and general Intensive Care Unit at Assiut university hospital. Sample: fifty patients admitted to trauma and general Intensive Care Unit. Tools: Four tools were used in this study, patient assessment tool, APACHE II tool, Acid-base parameters assessment tool, and Risk factors assessment tool. Result: A total of 50 patients most of them were male with a mean age of 40.37 ± 13.86 in the survivors versus 47.75 ± 11.86 in non-survivor. APACHE II score was significant in non-survivor group confirmed by (P = 0.000), (P = 0.003) respectively.The incidences of respiratory alkalosis (52%), respiratory acidosis (24%) were higher in the survivor group. The significant risk factor was iatrogenic(drugs, mechanical ventillation).Conclusion: Respiratory acid-base disorders are common in critically ill patients mainly respiratory alkalosis and the major related risk factor was an iatrogenic.

Acid-Base Disturbances in Patients with Asthma: A Literature Review and Comments on Their Pathophysiology.

Asthma is a common illness throughout the world that affects the respiratory system function, i.e., a system whose operational adequacy determines the respiratory gases exchange. It is therefore expected that acute severe asthma will be associated with respiratory acid-base disorders. In addition, the resulting hypoxemia along with the circulatory compromise due to heart–lung interactions can reduce tissue oxygenation, with a particular impact on respiratory muscles that have increased energy needs due to the increased workload. Thus, anaerobic metabolism may ensue, leading to lactic acidosis. Additionally, chronic hypocapnia in asthma can cause a compensatory drop in plasma bicarbonate concentration, resulting in non-anion gap acidosis. Indeed, studies have shown that in acute severe asthma, metabolic acid-base disorders may occur, i.e., high anion gap or non-anion gap metabolic acidosis. This review briefly presents studies that have investigated acid-base disorders in asthma, with comments on their underlying pathophysiology.

Adjusted Plasma Chloride and Bicarbonate Concentrations: An Approach to Identifying Acid–Base Disorders

Chloride disorders (hypochloremia, hyperchloremia) and bicarbonate disorders (hypobicarbonatemia, hyperbicarbonatemia) are common in clinical medicine and indicate metabolic and/or respiratory acid-base disorders. The normally inverse relationship between chloride and bicarbonate concentrations in the blood is altered, however, by changes in fluid balance, i.e., water excess or deficit, with resulting changes in sodium and other electrolyte concentrations and by anion gap metabolic acidosis, which lowers bicarbonate concentrations but not the chloride concentrations. We used formulas derived over a decade ago that utilize dry slide laboratory technology to adjust plasma chloride and bicarbonate concentrations for changes in water balance, as reflected in changes in plasma sodium concentrations and in the plasma anion gap. We then prospectively validated these formulas in 736 consecutive adults, 499 having abnormal basic metabolic panel results and 237 having normal panel results, using modern wet laboratory technology. Plasma chloride and bicarbonate concentrations were inversely correlated (2-tailed P-value <0.0001), but the correlations were only modest (Spearman r: -0.48 for the abnormal group and -0.41 for the normal group). After adjusting the plasma chloride and bicarbonate concentrations using the 2 prior formulas, the inverse correlations were very high, with Spearman r: -0.998 for the abnormal group and -0.999 for the normal group. Adjusting plasma chloride and bicarbonate concentrations for any water imbalance and anion gap alterations leads to very high inverse correlations between these 2 anions, allowing accurate assessment of either subtle or overt acid-base disorders.

Respiratory Acidosis and Alkalosis

Respiratory acid-base disorders are those disturbances in acid-base equilibrium that are expressed by a primary change in CO2 tension (Pco2) and reflect primary changes in the body’s CO2 stores (i.e., carbonic acid). A primary increase in Pco2 (and a primary increase in the body’s CO2 stores) defines respiratory acidosis or primary hypercapnia and is characterized by acidification of the body fluids. By contrast, a primary decrease in Pco2 (and a primary decrease in the body’s CO2 stores) defines respiratory alkalosis or primary hypocapnia and is characterized by alkalinization of the body fluids. Primary changes in Pco2 elicit secondary physiologic changes in plasma [HCO3ˉ] that are directional and proportional to the primary changes and tend to minimize the impact on acidity. This review presents the pathophysiology, secondary physiologic response, causes, clinical manifestations, diagnosis, and therapeutic principles of respiratory acidosis and respiratory alkalosis. This review contains 4 figures, 3 tables, and 59 references. Key words: Respiratory acidosis, respiratory alkalosis, primary hypercapnia, primary hypocapnia, hypoxemia, pseudorespiratory alkalosis

Respiratory Acidosis and Alkalosis

Respiratory acid-base disorders are those disturbances in acid-base equilibrium that are expressed by a primary change in CO2 tension (Pco2) and reflect primary changes in the body’s CO2 stores (i.e., carbonic acid). A primary increase in Pco2 (and a primary increase in the body’s CO2 stores) defines respiratory acidosis or primary hypercapnia and is characterized by acidification of the body fluids. By contrast, a primary decrease in Pco2 (and a primary decrease in the body’s CO2 stores) defines respiratory alkalosis or primary hypocapnia and is characterized by alkalinization of the body fluids. Primary changes in Pco2 elicit secondary physiologic changes in plasma [HCO3ˉ] that are directional and proportional to the primary changes and tend to minimize the impact on acidity. This review presents the pathophysiology, secondary physiologic response, causes, clinical manifestations, diagnosis, and therapeutic principles of respiratory acidosis and respiratory alkalosis. This review contains 4 figures, 3 tables, and 59 references. Key words: Respiratory acidosis, respiratory alkalosis, primary hypercapnia, primary hypocapnia, hypoxemia, pseudorespiratory alkalosis

Evaluation of the expected ventilatory response to metabolic acidosis in chronic hemodialysis patients.

Expected pCO2 during metabolic acidosis should be computed to rule out superimposing respiratory acid-base disorders, the latter being featured by too high or too low pCO2 than expected. At least 4 different and inconsistent formulas exist. Based on the common practical rule, the reduction of pCO2 equals 1.2 multiplied by the reduction of serum bicarbonate ([HCO3-]), whereas pCO2 equals to the 2 digit after pH decimal point according to Fulop. Instead, based on Winters' formula, pCO2 equals to 1.5 times [HCO3-] + 8. Finally, a very simple formula has been proposed, it reads pCO2 = [HCO3-] + 15. Beyond the evident simplicity, the latter has been effective in a small hemodialysis cohort but validation in a larger dataset is highly desirable. Formulas have been applied to 180 hemodialysis patients' blood samples dataset featured by mild metabolic acidosis (HCO3 ≥ 14 mEq/L) and root mean square errors (RMSE) associated with each formula were computed. pCO2 reference range was computed as expected pCO2 ± 2 RMSE. Fulop's rule and Winters' formula are associated with large prediction errors. Conversely, the common practical rule and the very simple formula are both featured by the same low error (1.7 mmHg). They further show good agreement and pick out the same reference range. Superimposing respiratory acid-base disorders can be promptly and effectively ruled out by computing expected pCO2 as [HCO3-] + 15, a very simple formula proved to be interchangeable with the common practical rule that requires computes and assumptions, but leads to same results.

Acid-Base Disorders

Anticipation and early identification of conditions that alter the body's ability to compensate for acid-base disorders are vital in managing surgical patients. This review describes the general principles and classification of acid-base disorders. Metabolic acid-base disorders are presented, including metabolic acidosis and alkalosis. Respiratory acid-base disorders are also presented, including respiratory acidosis and alkalosis. Tables show the differentiation of acid-base disorders, causes of positive–anion gap acidosis, the differential diagnosis for normal–anion gap metabolic acidosis, the mechanisms associated with increased serum lactate concentration, and the differential diagnosis for metabolic alkalosis. This review contains 7 highly rendered figures, 5 tables, and 135 references.

A mathematical model of blood-interstitial acid-base balance: application to dilution acidosis and acid-base status

We developed mathematical models that predict equilibrium distribution of water and electrolytes (proteins and simple ions), metabolites, and other species between plasma and erythrocyte fluids (blood) and interstitial fluid. The models use physicochemical principles of electroneutrality in a fluid compartment and osmotic equilibrium between compartments and transmembrane Donnan relationships for mobile species. Across the erythrocyte membrane, the significant mobile species Cl⁻ is assumed to reach electrochemical equilibrium, whereas Na(+) and K(+) distributions are away from equilibrium because of the Na(+)/K(+) pump, but movement from this steady state is restricted because of their effective short-term impermeability. Across the capillary membrane separating plasma and interstitial fluid, Na(+), K(+), Ca²(+), Mg²(+), Cl⁻, and H(+) are mobile and establish Donnan equilibrium distribution ratios. In each compartment, attainment of equilibrium by carbonates, phosphates, proteins, and metabolites is determined by their reactions with H(+). These relationships produce the recognized exchange of Cl(-) and bicarbonate across the erythrocyte membrane. The blood submodel was validated by its close predictions of in vitro experimental data, blood pH, pH-dependent ratio of H(+), Cl⁻, and HCO₃⁻ concentrations in erythrocytes to that in plasma, and blood hematocrit. The blood-interstitial model was validated against available in vivo laboratory data from humans with respiratory acid-base disorders. Model predictions were used to gain understanding of the important acid-base disorder caused by addition of saline solutions. Blood model results were used as a basis for estimating errors in base excess predictions in blood by the traditional approach of Siggaard-Andersen (acid-base status) and more recent approaches by others using measured blood pH and Pco₂ values. Blood-interstitial model predictions were also used as a basis for assessing prediction errors of extracellular acid-base status values, such as by the standard base excess approach. Hence, these new models can give considerable insight into the physicochemical mechanisms producing acid-base disorders and aid in their diagnoses.

Simple, easily memorised “rules of thumb” for the rapid assessment of physiological compensation for respiratory acid-base disorders

Respiratory acidosis and alkalosis are associated with compensatory physiological changes, including extracellular and intracellular buffering, and altered renal ion handling. In clinical practice, mixed acid-base disturbances may be misdiagnosed if...

Cross-Talk between Two Organs: How the Kidney Responds to Disruption of Acid-Base Balance by the Lung

Hypoventilation increases PaCO₂ (hypercapnia) and initiates the acid-base disorder known as respiratory acidosis. Hyperventilation decreases PaCO₂ (hypocapnia) and initiates the acid-base disorder known as respiratory alkalosis. The impact on acidity of these primary changes in PaCO₂ is ameliorated by secondary, directional changes in plasma bicarbonate concentration that occur in two stages. Acutely, modest changes in plasma bicarbonate originate from titration of the body’s nonbicarbonate buffers. In chronic hypercapnia and hypocapnia, larger changes in plasma bicarbonate occur that reflect adjustments in renal acidification mechanisms. As a result, the amelioration of systemic acidity is more pronounced in the chronic forms of the respiratory acid-base disorders.

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.

Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis.

In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis.

Na-HCO3 cotransport and Na-H antiporter in chronic respiratory acidosis and alkalosis

Renal acidification in renal proximal tubule is thought to be mediated by luminal Na-H antiporter and the HCO3- generated by this antiporter is removed from the cell by a basolateral Na-HCO3 cotransporter. To study the effect of respiratory acid-base disorders on these transport systems, we have measured the Na-HCO3 cotransport in basolateral membranes and Na-H antiporter in luminal membranes in control rabbits, rabbits exposed to 10% CO2 (chronic hypercapnia), and rabbits exposed to 10% O2-90% N2 (chronic hypocapnia). The Vmax of HCO3(-)-dependent 22Na uptake was significantly higher in chronic hypercapnia than controls (2.54 +/- 0.03 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.001). Likewise, the Vmax of the Na-H antiporter was also increased compared with controls (924.9 +/- 42.1 vs. 549.1 +/- 62.8 fluorescence units (FU).300 micrograms protein-1.min-1). In chronic hypocapnia, the Vmax of Na-HCO3 cotransport was lower than controls (0.72 +/- 0.11 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.05). There was no difference, however, in the Vmax of the Na-H antiporter between hypocapnia and control (524.2 +/- 24.3 vs. 549.1 +/- 62.8, FU.300 micrograms protein-1.min-1). The Vmaxs of the Na-HCO3 cotransport and of the Na-H antiporter in hypocapnic, control, and hypercapnic rabbits were linearly related (r = 0.81), suggesting a simultaneous adaptation of the two systems in respiratory acid-base disorders.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of collecting tubule hydrogen ion secretion in acute respiratory alkalosis using the urinary pCO2

The use of the urine-blood (U-B) pCO2 difference as a marker of collecting tubule H+ secretion (CTH+S) faces serious interpretative pitfalls when applied to animals with respiratory acidosis. The present study was aimed to examine the use of this parameter in rats with acute respiratory alkalosis. During infusion of sodium bicarbonate, the U-B pCO2 was only slightly lower in hypocapnic than in eucapnic rats (30 +/- 2.2 and 39 +/- 3.3 mmHg, p less than 0.05) and this difference was no longer significant when this parameter was examined as a function of urine bicarbonate concentration. In contrast, the increment in urine pCO2 elicited by bicarbonate loading (i.e. the delta pCO2) was markedly reduced in hypocapnic as compared to eucapnic rats (22 +/- 3.0 and 38 +/- 4.5 mmHg, respectively, p less than 0.01). The infusion of carbonic anhydrase while the urine was highly alkaline and the blood pCO2 kept constant resulted in a decrement in urine pCO2 which was less in hypocapnic than in eucapnic rats (-23.9 +/- 1.9 vs -33 +/- 2.8 mmHg, p less than 0.02). These findings indicate that pCO2 generation from CTH+S and titration of bicarbonate is reduced in hypocapnic rats. The data are in accord with our proposal that the delta pCO2 is a better index of CTH+S than the U-B pCO2 is the assessment of respiratory acid-base disorders.