Sodium Fate after Sodium Bicarbonate Infusion: Influence of Altered Acid-Base Status

2020 ◽  
Vol 51 (3) ◽  
pp. 182-191
Author(s):  
Horacio J. Adrogué ◽  
Ahmed A. Awan ◽  
Nicolaos E. Madias
Keyword(s):  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Hypertonic Solution ◽  
Acid Base ◽  
Pooled Data ◽  
Acid Base Status ◽  
Internal Distribution ◽  
Total Body ◽  
Bicarbonate Infusion ◽  
Initial Blood

Background: We have previously investigated the fate of administered bicarbonate infused as a hypertonic solution in animals with each of the 4 chronic acid-base disorders. Those studies did not address the fate of sodium, the coadministered cation. Methods: We examined baseline total body water (TBW), Na+ space, HCO3– space, and urinary sodium and bicarbonate excretion after acute hypertonic NaHCO3 infusion (1-N solution, 5 mmol/kg body weight) in dogs with each of the 4 chronic acid-base disorders. Observations were made at 30, 60, and 90 min postinfusion. Retained sodium that remains osmotically active distributes in an apparent space that approximates TBW. Na+ space that exceeds TBW uncovers nonosmotic sodium storage. Results: Na+ space approximated TBW at all times in normal and hyperbicarbonatemic animals (metabolic alkalosis and respiratory acidosis), but exceeded TBW by ~30% in hypobicarbonatemic animals (metabolic acidosis and respiratory alkalosis). Such osmotic inactivation was detected at 30 min and remained stable. The pooled data revealed that Na+ space corrected for TBW was independent of the initial blood pH but correlated with initial extracellular bicarbonate concentration (y = –0.01x + 1.4, p= 0.002). The fate of administered sodium and bicarbonate (internal distribution and urinary excretion) was closely linked. Conclusions: This study demonstrates that hypobicarbonatemic animals have a Na+ space that exceeds TBW after an acute infusion of hypertonic NaHCO3 indicating osmotic inactivation of a fraction of retained sodium. In addition to an expanded Na+ space, these animals have a larger HCO3– space compared with hyperbicarbonatemic animals. Both phenomena appear to reflect the wider range of titration of nonbicarbonate buffers (Δ pH) occurring during NaHCO3– loading whenever initial [HCO3–]e is low. The data indicate that the fate of administered bicarbonate drives the internal distribution and the external disposal of sodium, the co-administered cation, and is responsible for the early, but non-progressive, osmotic inactivation of a fraction of the retained sodium.

Influence of chronic respiratory acid-base disorders on acute CO2 titration curve

1985 ◽  
Vol 58 (4) ◽  
pp. 1231-1238 ◽  
Author(s):  
H. J. Adrogue ◽  
N. E. Madias
Keyword(s):  
Titration Curve ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Ion Concentration ◽  
Whole Body ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Plasma Bicarbonate ◽  
Base Disorder ◽  
Acid Base Status

We have recently shown that background presence of chronic metabolic acid-base disorder markedly alters in vivo acute CO2 titration curve. These studies were carried out to assess the influence of chronic respiratory acid-base disorders on response to acute hypercapnia and to explore whether the chronic level of plasma pH is the factor responsible for alterations in the CO2 titration curve. We compared whole-body responses to acute hypercapnia of dogs with preexisting chronic respiratory alkalosis (n = 8) with that of normal animals (n = 4) and animals with chronic respiratory acidosis (n = 13). Chronic respiratory alkalosis and acidosis, as well as the acute CO2 titrations, were produced in unanesthetized dogs within a large environmental chamber. For comparison with our data on chronic metabolic acidosis and alkalosis, plasma bicarbonate levels, which are secondarily altered in chronic respiratory acid-base disorders, were used as an index of chronic acid-base status of the animals. Results indicate that, as with chronic metabolic acid-base disorders, a larger increment in plasma bicarbonate occurs during acute hypercapnia when steady-state plasma bicarbonate is low (respiratory alkalosis) than when it is high (respiratory acidosis). Yet, in further analogy with the metabolic studies, plasma hydrogen ion concentration is better defended at higher plasma bicarbonate levels in accordance with mathematical relationships defined by the Henderson-Hasselbalch equation. Combined results demonstrate that the influence of chronic acid-base status on whole-body response to acute hypercapnia is independent of initial plasma pH.

Respiratory Acidosis and Alkalosis

2017 ◽  
Author(s):  
Horacio J Adrogué ◽  
Nicolaos E Madias
Keyword(s):  
Carbonic Acid ◽  
Clinical Manifestations ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Body Fluids ◽  
The Body ◽  
Acid Base ◽  
Acid Base Equilibrium ◽  
Therapeutic Principles ◽  
The Impact

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

Exercise and forced submergence in the pond slider (Trachemys scripta) and softshell turtle (Apalone ferox): influence on bimodal gas exchange, diving behaviour and blood acid-base status

1999 ◽  
Vol 202 (3) ◽  
pp. 267-278 ◽  
Author(s):  
B. Bagatto ◽  
R.P. Henry
Keyword(s):  
Gas Exchange ◽  
Metabolic Stress ◽  
Respiratory Acidosis ◽  
Diving Behaviour ◽  
Trachemys Scripta ◽  
Acid Base ◽  
Aerial Respiration ◽  
Acid Base Status ◽  
Softshell Turtle ◽  
Apalone Ferox

The dynamics of bimodal respiration, diving behaviour and blood acid-base status in the softshell turtle Trachemys scripta and the pond slider Apalone ferox were investigated at rest and under conditions of stress induced by exercise and forced submergence. During periods of forced submergence, only A. ferox doubled its aquatic gas exchange rate. Both A. ferox and T. scripta increased their aerial gas exchange profoundly following exercise and forced submergence, a pattern indicative of increased anaerobic respiration. Emersion duration increased significantly in A. ferox following forced submergence, and mean apnoeic time decreased significantly in A. ferox following exercise, indicating that a larger proportion of time at the surface was spent ventilating. Also, A. ferox maintained a one-breath breathing bout regardless of treatment. Submergence produced a respiratory acidosis in the plasma of approximately 0.2 pH units in magnitude in T. scripta and a mixed respiratory/metabolic acidosis of 0.4 pH units in A. ferox. Exercise induced an acidosis of 0.2 pH units of primarily metabolic origin in both species. Intra-erythrocyte pH was also reduced in both species in response to submergence and exercise. Both intracellular and extracellular acidoses were more severe and longer lasting in A. ferox after each treatment. Plasma [HCO3-] decreased by 25 % in both species following exercise, but only in A. ferox following submergence. Plasma lactate concentrations increased by equal amounts in each species following exercise; however, they returned to resting concentrations sooner in T. scripta than in A. ferox. A. ferox had significantly higher lactate levels than T. scripta following forced submergence as well as a slower recovery time. A. ferox, which is normally a good bimodal gas exchanger at rest, utilizes aerial respiration to a greater extent when under respiratory and/or metabolic stress. T. scripta, although almost entirely dependent on aerial respiration, is physiologically better able to deal with the respiratory and metabolic stresses associated with both forced submergence and exercise.

Studies on the Pathophysiology of Encephalopathy in Reye's Syndrome: Hyperammonemia in Reye's Syndrome

PEDIATRICS ◽  
1975 ◽  
Vol 56 (6) ◽  
pp. 999-1004
Author(s):  
Daniel C. Shannon ◽  
Robert De Long ◽  
Barry Bercu ◽  
Thomas Glick ◽  
John T. Herrin ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Venous Drainage ◽  
Respiratory Alkalosis ◽  
Ammonia Concentration ◽  
Reye's Syndrome ◽  
Acid Base ◽  
Arterial Blood ◽  
Cerebral Venous Drainage ◽  
Acid Base Status ◽  
The Brain

The initial acid-base status of eight survivors of Reye's syndrome was characterized by acute respiratory alkalosis (Pco2=32 mm Hg; Hco3-= 22.0 mEq/liter) while that of eight children who died was associated with metabolic acidosis as well (HCO3-=10.0 mEq/liter). Arterialinternal jugular venous ammonia concentration differences on day 1 (299 mg/100 ml) and day 2 (90 mg/ 100 ml) reflected cerebral uptake of ammonia while those on days 3 and 4 (-43 and -55 mg/100 ml) demonstrated cerebral release. Arterial blood hyperammonemia can be detoxified safely in the brain as long as the levels do not exceed approximately 300µg/100 ml. Beyond that level lactic acidosis is observed, particularly in cerebral venous drainage. Arterial blood hyperammonemia was also related to the extent of alveolar hyperventilation. These findings are very similar to those seen in experimental hyperammonemia and support the concept that neurotoxicity in children with Reye's syndrome is at least partly due to impaired oxidative metabolism secondary to hyperammonemia.

Stability of cerebrospinal fluid pH in chronic acid-base disturbances in blood

1965 ◽  
Vol 20 (3) ◽  
pp. 443-452 ◽  
Author(s):  
R. A. Mitchell ◽  
C. T. Carman ◽  
J. W. Severinghaus ◽  
B. W. Richardson ◽  
M. M. Singer ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Active Transport ◽  
Respiratory Acidosis ◽  
Normal Subjects ◽  
Respiratory Alkalosis ◽  
Regulation Of Respiration ◽  
Respiratory Drive ◽  
Acid Base ◽  
Peripheral Chemoreceptors ◽  
Mean Values

In chronic acid-base disturbances, CSF pH was generally within the normal limits (7.30–7.36 units, being the range including two standard deviations of 12 normal subjects). The mean values of CSF and arterial pHH, respectively, were: 1) metabolic alkalosis, 7.337 and 7.523; 2) metabolic acidosis, 7.315 and 7.350; 3) respiratory alkalosis, 7.336 and 7.485; and 4) respiratory acidosis (untreated), 7.314 and 7.382. Other investigators report similar values. The constancy of CSF pH cannot be explained by a poorly permeable blood-CSF barrier in chronic metabolic acidosis and alkalosis, nor can it be explained by respiratory compensation. It cannot be explained by renal compensation in respiratory alkalosis (high altitude for 8 days), although it may be explained by renal compensation in respiratory acidosis. The former three states suggest that active transport regulation of CSF pH is a function of the blood-CSF barrier. Since CSF pH is constant, so also must that portion of the respiratory drive originating in the superficial medullary respiratory chemoreceptors be constant. Ventilation changes in chronic acid-base disturbances thus may result from changes in the activity of peripheral chemoreceptors, in response to changes in arterial pH, arterial PO2, and possibly in neuromuscular receptors. regulation of respiration; medullary respiratory; chemoreceptors; peripheral chemoreceptors; metabolic acidosis and alkalosis; respiratory acidosis and alkalosis; active transport; blood-brain barrier; pregnancy Submitted on July 27, 1964

Practical Evaluation of Acid-Base Balance

1957 ◽  
Vol 3 (5) ◽  
pp. 631-637
Author(s):  
Herbert P Jacobi ◽  
Anthony J Barak ◽  
Meyer Beber
Keyword(s):  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Acid Base Balance ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Practical Evaluation ◽  
Base Balance

Abstract The Co2 combining power bears a variable relationship to the in vivo plasma bicarbonate concentration, depending upon the type and severity of acid-base distortion. In respiratory alkalosis and metabolic acidosis the Co2 combining power will usually be greater than the in vivo plasma bicarbonate concentration; whereas, in respiratory acidosis and metabolic alkalosis the Co2 combining power will usually be less. Co2 content, on the other hand, will always parallel the in vivo plasma bicarbonate concentration quite closely, being only slightly greater. These facts, together with other considerations which are discussed, recommend the abandonment of the determination of CO2 combining power.

Anesthetic effects on liver and muscle glycogen concentrations: rest and postexercise

1989 ◽  
Vol 66 (6) ◽  
pp. 2895-2900 ◽  
Author(s):  
T. I. Musch ◽  
B. S. Warfel ◽  
R. L. Moore ◽  
D. R. Larach
Keyword(s):  
Skeletal Muscles ◽  
Respiratory Acidosis ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Acid Base ◽  
Arterial Lactate ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Gastrocnemius Muscles

We compared the effects of three different anesthetics (halothane, ketamine-xylazine, and diethyl ether) on arterial blood gases, acid-base status, and tissue glycogen concentrations in rats subjected to 20 min of rest or treadmill exercise (10% grade, 28 m/min). Results demonstrated that exercise produced significant increases in arterial lactate concentrations along with reductions in arterial Pco2 (PaCO2) and bicarbonate concentrations in all rats compared with resting values. Furthermore, exercise produced significant reductions in the glycogen concentrations in the liver and soleus and plantaris muscles, whereas the glycogen concentrations found in the diaphragm and white gastrocnemius muscles were similar to those found at rest. Rats that received halothane and ketamine-xylazine anesthesia demonstrated an increase in Paco2 and a respiratory acidosis compared with rats that received either anesthesia. These differences in arterial blood gases and acid-base status did not appear to have any effect on tissue glycogen concentrations, because the glycogen contents found in liver and different skeletal muscles were similar to one another cross all three anesthetic groups. These data suggest that even though halothane and ketamine-xylazine anesthesia will produce a significant amount of ventilatory depression in the rat, both anesthetics may be used in studies where changes in tissue glycogen concentrations are being measured and where adequate general anesthesia is required.

The influence of respiratory acid-base changes on muscle performance and excitability of the sarcolemma during strenuous intermittent hand grip exercise

2012 ◽  
Vol 112 (4) ◽  
pp. 571-579 ◽  
Author(s):  
M. Hilbert ◽  
V. Shushakov ◽  
N. Maassen
Keyword(s):  
Force Production ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Muscle Performance ◽  
Protective Effects ◽  
Acid Base ◽  
M Wave ◽  
Hand Grip

Acidification has been reported to provide protective effects on force production in vitro. Thus, in this study, we tested if respiratory acid-base changes influence muscle function and excitability in vivo. Nine subjects performed strenuous, intermittent hand grip exercises (10 cycles of 15 s of work/45 s of rest) under respiratory acidosis by CO2 rebreathing, alkalosis by hyperventilation, or control. The Pco2, pH, K+ concentration ([K+]), and Na+ concentration were measured in venous and arterialized blood. Compound action potentials (M-wave) were elicited to examine the excitability of the sarcolemma. The surface electromyogram (EMG) was recorded to estimate the central drive to the muscle. The lowest venous pH during the exercise period was 7.24 ± 0.03 in controls, 7.31 ± 0.05 with alkalosis, and 7.17 ± 0.04 with acidosis ( P < 0.001). The venous [K+] rose to similar maximum values in all conditions (6.2 ± 0.8 mmol/l). The acidification reduced the decline in contraction speed ( P < 0.001) but decreased the M-wave area to 73.4 ± 19.8% ( P < 0.001) of the initial value. After the first exercise cycle, the M-wave area was smaller with acidosis than with alkalosis, and, after the second cycle, it was smaller with acidosis than with the control condition ( P < 0.001). The duration of the M-wave was not affected. Acidification diminished the reduction in performance, although the M-wave area during exercise was decreased. Respiratory alkalosis stabilized the M-wave area without influencing performance. Thus, we did not find a direct link between performance and alteration of excitability of the sarcolemma due to changes in pH in vivo.

scholarly journals Effects of Environmental Heat and Intake of Tall Fescue Seed Infested with Acremonium Coenophialum on the Acid-Base Status of Young Bulls

1996 ◽  
Vol 8 (2) ◽  
pp. 233-237 ◽  
Author(s):  
L. L. Mills Wallace ◽  
D. W. Vogt ◽  
R. J. Lipsey ◽  
G. B. Gamer ◽  
C. N. Cornell
Keyword(s):  
Heat Stress ◽  
Tall Fescue ◽  
Festuca Arundinacea ◽  
Environmental Temperature ◽  
Respiratory Alkalosis ◽  
Acremonium Coenophialum ◽  
Acid Base ◽  
Arterial Blood ◽  
Metabolic Compensation ◽  
Acid Base Status

Effects of high environmental temperature and dietary intake of tall fescue ( Festuca arundinacea) seed containing the endophyte Acremonium coenophialum on bovine acid-base status were studied using 3 groups of bull calves (2 Simmental, 1 Angus). Experimental animals were housed in controlled-climate chambers and subjected to gradual increases in environmental temperature, first while being fed an endophyte-free diet and then while being fed a diet containing 17% endophyte-infested fescue seed. Marked acid-base disturbances were not observed in any animals. In general, Pco2, HCO3-, base excess, and arterial blood pH values were reduced in response to heat stress, both with endophyte-free and endophyte-containing diets. In most individuals anion gap increased. These results reflected metabolic compensation for mild chronic alveolar hyperventilation and retention of organic acids. These findings suggest that, under conditions similar to those found during the summer in central Missouri, normal cattle should not be at great risk of developing respiratory alkalosis or other severe acid-base disturbances as a result of heat stress and/or intake of tall fescue endophyte.

scholarly journals The effects of post-operative oxygen supply on blood oxygenation and acid-base status in rats anaesthetized with fentanyl/fluanisone and midazolam

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0255829
Author(s):  
Leander Gaarde ◽  
Stefanie Kolstrup ◽  
Peter Bollen
Keyword(s):  
Oxygen Saturation ◽  
Oxygen Supply ◽  
Respiratory Acidosis ◽  
Blood Oxygenation ◽  
Acid Base ◽  
Blood Oxygen Saturation ◽  
Arterial Blood ◽  
Post Operative Period ◽  
Significant Difference ◽  
Acid Base Status

In anaesthetic practice the risk of hypoxia and arterial blood gas disturbances is evident, as most anaesthetic regimens depress the respiratory function. Hypoxia may be extended during recovery, and for this reason we wished to investigate if oxygen supply during a one hour post-operative period reduced the development of hypoxia and respiratory acidosis in rats anaesthetized with fentanyl/fluanisone and midazolam. Twelve Sprague Dawley rats underwent surgery and were divided in two groups, breathing either 100% oxygen or atmospheric air during a post-operative period. The peripheral blood oxygen saturation and arterial acid-base status were analyzed for differences between the two groups. We found that oxygen supply after surgery prevented hypoxia but did not result in a significant difference in the blood acid-base status. All rats developed respiratory acidosis, which could not be reversed by supplemental oxygen supply. We concluded that oxygen supply improved oxygen saturation and avoided hypoxia but did not have an influence on the acid-base status.

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