Blood Acid-base Variables Research Articles

Comparison of mild physiological effects of surgical masks and N95 respirators over 60 min at rest.

Dead-space-associated rebreathing of expired air and heat trapping with use of surgical masks and N95 respirators may underlie anecdotal reports of adverse symptoms associated with medical face barriers. Limited data exist directly comparing the physiological effects of masks and respirators at rest. We assessed the short-term physiological effects of both barrier types over 60 min at rest, including face microclimate temperature, end-tidal gases, and venous blood acid-base variables. We recruited 34 participants into two trials: surgical masks (n = 17) and N95 respirators (n = 17). In a seated position, participants underwent a 10-min baseline without a barrier and then wore a standardized surgical mask or dome-shaped N95 respirator for 60 min, followed by a 10-min washout. We instrumented healthy human participants with a peripheral pulse oximeter ([Formula: see text]) and a nasal cannula connected to a dual gas analyzer for measurement of the pressure of end-tidal [Formula: see text] and [Formula: see text], with an associated temperature probe for face microclimate temperature. Venous (v) blood samples were obtained at baseline and following 60-min mask/respirator wearing to assess [Formula: see text], [HCO3-]v and pHv. Compared with baseline during/following 60 min, temperature, [Formula: see text], [Formula: see text], and [HCO3-]v were mildly but significantly higher, and [Formula: see text] and [Formula: see text] were significantly lower, but [Formula: see text] was unaffected. The magnitude of effects was similar between barrier types. Temperature and [Formula: see text] returned to baseline levels within 1-2 min following removal of the barrier. These mild physiological effects may underlie reports of qualitative symptoms while wearing masks or respirators. However, the magnitudes were mild, not physiologically relevant and reversed immediately with the removal of the barrier.NEW & NOTEWORTHY Anecdotal reports suggest mild physiological effects of wearing surgical masks and/or N95 respirators, including heat trapping and rebreathing of expired air. There are limited data directly comparing the physiological effects of wearing medical barriers at rest. We found that the time course and magnitude of changes to face microclimate temperature, end-tidal gases, and venous blood gases and acid-base variables were mild in magnitude, not physiologically relevant, equivalent between barrier types, and immediately reversible on removal.

The Reproducibility of 4-km Time Trial (TT) Performance Following Individualised Sodium Bicarbonate Supplementation: a Randomised Controlled Trial in Trained Cyclists

BackgroundIndividual time to peak blood bicarbonate (HCO3−) has demonstrated good to excellent reproducibility following ingestion of both 0.2 g kg−1 body mass (BM) and 0.3 g kg−1 BM sodium bicarbonate (NaHCO3), but the consistency of the time trial (TT) performance response using such an individualised NaHCO3 ingestion strategy remains unknown. This study therefore evaluated the reproducibility of 4-km TT performance following NaHCO3 ingestion individualised to time to peak blood bicarbonate.MethodsEleven trained male cyclists completed five randomised treatments with prior ingestion of 0.2 g kg−1 (SBC2) or 0.3 g kg−1 BM (SBC3) NaHCO3, on two separate occasions each, or a control trial entailing no supplementation. Participants completed a 4-km cycling TT on a Velotron ergometer where time to complete, power and speed were measured, whilst acid-base blood parameters were also recorded (pH and blood bicarbonate concentration HCO3−) and lactate [La−].ResultsAlkalosis was achieved prior to exercise in both SBC2 and SBC3, as pH and HCO3− were greater compared to baseline (p < 0.001), with no differences between treatments (p > 0.05). The reproducibility of the mean absolute change from baseline to peak in HCO3− was good in SBC2 (r = 0.68) and excellent in SBC3 (r = 0.78). The performance responses following both SBC2 and SBC3 displayed excellent reproducibility (r range = 0.97 to 0.99).ConclusionsResults demonstrate excellent reproducibility of exercise performance following individualised NaHCO3 ingestion, which is due to the high reproducibility of blood acid-base variables with repeat administration of NaHCO3. Using a time to peak HCO3- strategy seems to cause no dose-dependent effects on performance for exercise of this duration and intensity; therefore, athletes may consider smaller doses of NaHCO3 to mitigate gastrointestinal (GI) discomfort.

Blood acid–base changes during acute experimental inflammation in rats

Acidosis has often been reported in inflamed tissues, and changes in strong relevant ions at the site of inflammation may provoke alterations in blood acid-base status. We measured changes in blood acid-base variables during carrageenan-induced inflammation in rats. We found a mixed acid-base disorder in rat blood during acute inflammation (12, 24, and 48 h). A metabolic acid contribution was found during the first 12 h and maintained further, as revealed by a decrease in plasma strong ion concentration difference ([SID]) and an increase in plasma weak acid concentration due to a rise in inorganic phosphate ([ATOT]P(i)). Plasma [SID] and [ATOT]P(i) changes were probably due to exchange of Na+ and P(i) between the inflammatory exudate and rat blood. A secondary respiratory compensation for the metabolic acid changes occurred in the blood of inflamed rats, resulting in significant hypocapnia. Furthermore, a progressive decrease in the total weak acid buffer concentration due to a decrease in plasma albumin ([ATOT]Alb) also counteracted the impact of changes in [SID] and P(i) to increase blood acidity. Therefore, despite the metabolic acid-base disorders induced by inflammatory processes, hydrogen ion (H+) homeostasis was maintained, and blood pH remained essentially unchanged in the inflamed rats.

Differential Approaches to Blood Acid-Base Regulation during Exposure to Prolonged Hypercapnia in Two Freshwater Teleosts: The Rainbow Trout (Salmo gairdneri) and the American Eel (Anguilla rostrata)

The effects of external hypercapnia (0.8% CO₂ in air) on blood acid-base variables were examined in the eel (Anguilla rostrata) and in the trout (Salmo gairdneri). Both species were able topartially regulate whole-bloodpH during hypercapnia owing to similar elevations ofplasma [HCO₃-]. In the trout, the ability to regulate whole-blood pH was attributed primarily to a reduction in the activity of branchial Cl⁻/HCO₃-exchange, whereas, in the eel, pH regulation was due entirely to stimulation of branchial Na⁺/H⁺ exchange. Acclimation of eels to increased external [NaCl] (2 mM) caused a significant blood alkalosis; branchial Na⁺ uptake was markedly stimulated (from 34 to 921 μmol kg⁻¹ h⁻¹), while Cl⁻ uptake remained at exceptionally low levels (5-6μmol kg⁻¹ h⁻¹). However, the ability to regulate hypercapnic acidosis in eels acclimated to high [NaCl] water was unchanged. Eels also were acclimated to low external [Na⁺] (Na⁺ = 0.0090 ± 0.0003 mM; Cl⁻ = 0.162 ± 0.017 mM), which resulted in a significant decrease in whole-blood pH. Branchial Na⁺ uptake was markedly reduced (from 34 to 8 μ mol kg⁻¹ h⁻¹), and the ability to compensate hypercapnic acidosis was abolished. These data indicate that, unlike the trout, the eel relies solely on adjustments of branchial Na⁺ uptake for blood acid-base regulation during hypercapnic acidosis owing to uniquely low and inflexible rates of gill unidirectional Cl⁻ fluxes.

Bisphosphonates and extrarenal acid buffering capacity

Both the intracellular compartment and bone mineral are supposed to play a role in acid-base balance by contributing to the extrarenal acid buffering capacity. Bisphosphonates could affect extrarenal acid buffering capacity by interfering with the formation and/or dissolution of bone mineral. In the present study, rats were pretreated with either 1-hydroxyethylidene-1, 1-bisphosphonate (HEBP, 10 mg/kg.day sc), with prevailing inhibitory action on bone mineral formation, or dichloromethylene bisphosphonate (Cl2MBP, 10 mg p/kg.day sc) with prevailing action on bone resorption, or NaCl injections (controls) for 7 days. In intact rats, blood acid-base variables were influenced by neither HEBP, nor Cl2MBP. Two hours after nephrectomy and before acute acid loading, HEBP-but not Cl2MBP-pretreated rats displayed a significant increase in both blood HCO3- and PCO2. After HCl infusion (2.5 mEq/kg), the relative decrement in blood HCO3- (difference in blood HCO3- before and after acid loading) was transiently more important in the two bisphosphonate pretreated groups than in controls. After a 24 hour fasting period, nephrectomized animals pretreated with Cl2MBP displayed significantly lower blood HCO3- and pH values than controls or HEBP-pretreated rats. These results suggest that bisphosphonates influence extrarenal buffering capacity according to their prevailing inhibitory action on either bone mineral formation and/or dissolution. These compounds could interfere with the release rate of bone proton buffers. However, in the presence of normal renal function, this effect does not disturb the blood acid-base equilibrium.

Acetazolamide and cerebrospinal fluid ions in drugs with normal acid-base balance

The purpose of these experiments was to study the effects of acetazolamide, a carbonic anhydrase inhibitor, on cisternal cerebrosphinal fluid (CSF) ions during normal acid-base balance. We measured blood and CSF acid-base variables in two groups (n = 6 in each) of anesthetized, paralyzed and mechanically ventilated dogs with bilateral ligation of renal pedicles. After baseline samples were obtained, acetazolamide was administered intravenously within 10 min (group II); group I received equal volume (20 ml) of half-normal saline. During the next 6 h, in both groups arterial blood acid-base variables and plasma strong ions remained relatively normal. In group I, mean values for cisternal CSF P CO 2 were 45.3 and 49.3 mm Hg at 0 and 6 h; respective values for CSF [HCO 3 −] were 24.1 and 22.7 mEq/L. In group II, corresponding values for P CO 2 and [HCO 3 −] were 46.4 and 51.9 mm Hg, adn 23.8 and 23.7 mEq/L. respectively. Comparing the two groups, related mean values were not significantly different from each other. Futhermore, acetazolamide had no significant effect of CSF Na +, K + and Cl − concentrations. Based on the results of this study and those reported previously, we conclude that under normal acid-base balance, acetazolamide does not change ionic composition of cisternal CSF, choroidal CSF or brain extracellular fluid.

The effect of sodium bicarbonate or potassium bicarbonate on acid-base status and protein and energy digestibility in swine

Three experiments were conducted to evaluate the effects of Na or K on acid-base status and nutrient utilization in young growing pigs. These studies were carried out to develop a better understanding of the growth response to alkaline salts of these minerals that have been observed in lysine-deficient swine. In experiment 1, a 2×2 factorial arrangement of 2.2 g/kg vs. 7.4 g/kg Na and ad libitum vs. meal feeding regimens was used to evaluated the effects of Na on blood acid-base variables. Na was supplemented as the alkaline salt, NaHCO 3. For each treatment regimen, blood samples were collected via indwelling vena cava catheters every 2 hr for 28 hr. Sodium supplementation increased (P<0.05) blood HCO 3 − and base excess and tended (P<0.07) to increase pH. Plasma urea N was depressed (P<0.05) by the meal feeding regimen. In experiment 2, the effect of NaHCO 3 (1.3% or 2.6%) or KHCO 3 (3.0%) on apparent nutrient digestibility and nitrogen balance was investigated utilizing pigs fitted with simple T cannulas in the ileum near the ileocecal junction. A 4×4 Latin square design was used. KHCO 3 or 2.6% NaHCO 3 increased (P<0.05) urinary volume and increased (P<0.05) urine pH. NaHCO 3 had no effect (P<0.05) on apparent digestibility of lysine, tryptophan, nitrogen or energy or on nitrogen balance. KHCO 3 decreased (P<0.05) energy digestibility. In experiment 3, the effect of 2.6% NaHCO 3 on gastrointestinal pH was studied. No effects (P>0.05) were observed in the stomach, duodenum, jejunum, ileum, cecum or colon. NaHCO 3 or KHCO 3 alter the acid-base balance of the pig. However, their growth-promoting effects in lysine-deficient pigs are not due to enhanced lysine or protein digestibility

Changes in the brain surface pH and cisternal cerebrospinal fluid acid-base variables in respiratory arrest

Using flat-surface pH electrodes we continuously measured changes in the brain surface pH during respiratory arrest in anesthetized and paralyzed dogs which were previously ventilated with pure oxygen. Respiratory arrest was induced by halting the respirator. The mean arterial Po2 fell from 502.7 ± 15.9 (1SD) to 23.7 ± 18.5, and the mean arterial Pco~, rose from 36.4 ± 80.4 ± 7.1mm Hg, 10 min after asphyxia. The arterial blood pressure increased gradually over several minutes but fell relatively abruptly and profoundly at the end, due to circulatory failure. Initially, and as long as the arterial blood pressure and, therefore, cerebral blood flow were upheld (phase 1), changes in the brain surface pH were small (ΔpH/Δt= −0.026 pH unit/min) in spite of severe hypercapnia. When cerebral perfussion pressure fell due to circulatory failure (phase 2), cerebral ischemia occurred and there was an abrupt fall in brain surface pH (Δph/Δt= −0.067pH unit/min). Changes in cisternal CSF [H +] grossly underestimated the magnitude of brain surface acidosis during the period of respiratory arrest; the initial difference between the mean brain surface fluid and cisternal CSF [H +] which was 8.9, rose to 15.1 and 47.4 nmol/L, respectively, 5 and 10 min after asphyxia. Changes in sagittal venous blood acid-base variables were more pronounced than those observed in the arterial blood or cisternal CSF; 5 min after respiratory arrest, arterial and sagittal venous blood and cisternal CSF and brain surface pH were 7.20, 7.09, 7.19, and 7.11, respecitvely. We conclude that (1) in the course of respiratory arrest cerebral outcome can potentially be determined by circulatory failure as evidenced by simultaneous changes in the arterial blood pressure and brain surface pH; (2) cisternal CSF acid-base changes lag behind those on the brain surface and CSF analyses provide unreliable information about the severity of brain acid-base changes during asphyxia; (3) changes in cerebral venous blood acid-base variables best represent the severity of metabolic aberrations in the brain during respiratory arrest.

Temperature-induced changes in turtle CSF pH and central control of ventilation

Cerebrospinal fluid (CSF) and arterial blood acid-base variables, as well as respiratory minute volume (RMV), were measured at three different body temperatures in unanesthetized turtles. RMV remained constant while CSF pH decreased 0.015 U/°C with increasing body temperature. These results show that ventilation is not tracking CSF pH when body temperature is the independent variable; however, perfusion of the brain ventricular system of turtles with mock CSF, in which ion-dependent pH decreases were produced, caused large increases in ventilation which were independent of body temperature. Comparisons between turtles and goats reveal that central chemical control of ventilation is functioning similarly in the two animals and appears to fit the alphastat model of ventilary control proposed by Reeves. These data strongly suggest that both animals are maintaining the fractional dissociation of imidazole constant in central receptive structures, indicating that this system is the model for central chemical control of ventilation in air-breathing vertebrates.