Time Course and Magnitude of Ventilatory and Renal Acid-Base Acclimatization Following Rapid Ascent to and Residence at 3,800 m over Nine Days

2021 ◽  
Author(s):  
Jordan D. Bird ◽  
Jack K. Leacy ◽  
Glen Edward Foster ◽  
Caroline A. Rickards ◽  
Richard J.A. Wilson ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
High Altitude ◽  
Time Course ◽  
Respiratory Alkalosis ◽  
High Gain ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Renal Response ◽  
Arterial Ph ◽  
Rapid Ascent

Rapid ascent to high altitude imposes an acute hypoxic and acid-base challenge, with ventilatory and renal acclimatization countering these perturbations. Specifically, ventilatory acclimatization improves oxygenation, but with concomitant hypocapnia and respiratory alkalosis. A compensatory, renally-mediated relative metabolic acidosis follows via bicarbonate elimination, normalizing arterial pH(a). The time-course and magnitude of these integrated acclimatization processes are highly variable between individuals. Using a previously-developed metric of renal reactivity (RR), indexing the change in arterial bicarbonate concentration (∆[HCO3-]a; renal response) over the change in arterial pressure of CO2 (∆PaCO2; renal stimulus), we aimed to characterize changes in RR magnitude following rapid ascent and residence at altitude. Resident lowlanders (n=16) were tested at 1,045 m (Day [D]0) prior to ascent, on D2 within 24-hours of arrival, and D9 during residence at 3,800 m. Radial artery blood draws were obtained to measure acid-base variables: PaCO2, [HCO3-]a and pHa. Compared to D0, PaCO2 and [HCO3-]a were lower on D2 (P<0.01) and D9 (P<0.01), whereas significant changes in pHa (P>0.058) and RR (P=0.056) were not detected. As pHa appeared fully compensated on D2 and RR did not increase significantly from D2 to D9, these data demonstrate renal acid-base compensation within 24-hours at moderate steady-state altitude. Moreover, RR was strongly and inversely correlated with ∆pHa on D2 and D9 (r≤-0.95; P<0.0001), suggesting that a high-gain renal response better protects pHa. Our study highlights the differential time-course, magnitude, and variability of integrated ventilatory and renal acid-base acclimatization following rapid ascent and residence at high altitude.

Cerebral acid-base and gas metabolism in brain injury

1970 ◽  
Vol 33 (5) ◽  
pp. 498-505 ◽  
Author(s):  
R. Zupping
Keyword(s):  
Metabolic Acidosis ◽  
Brain Injury ◽  
Brain Damage ◽  
Close Correlation ◽  
Respiratory Alkalosis ◽  
Acid Base ◽  
Content Type ◽  
Arterial Blood ◽  
Gas Metabolism ◽  
Permanent Brain Damage

✓ Acid-base and gas parameters of CSF, jugular venous and arterial blood were measured in 45 patients with brain injury in the first 12 days after trauma or operation. CSF metabolic acidosis together with respiratory alkalosis and hypoxemia in the cerebral venous and arterial blood were the most characteristic findings. A close correlation between the severity of brain damage and the intensity of the CSF metabolic acidosis and arterial hypocapnia was revealed. It was concluded that brain hypoxia and acidosis play an important role in the development of cerebral edema and permanent brain damage.

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.

Role of endothelin-1 in renal regulation of acid-base equilibrium in acidotic humans

2012 ◽  
Vol 303 (7) ◽  
pp. F991-F999 ◽  
Author(s):  
Alexandra Pallini ◽  
Henry N. Hulter ◽  
Jurgen Muser ◽  
Reto Krapf
Keyword(s):  
Metabolic Acidosis ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Endothelin 1 ◽  
Plasma Bicarbonate ◽  
Human Volunteers ◽  
Acid Base Equilibrium ◽  
Normal Human ◽  
Mineralocorticoid Activity

Endothelin-1 inhibits collecting duct sodium reabsorption and stimulates proximal and distal tubule acidification in experimental animals both directly and indirectly via increased mineralocorticoid activity. Diet-induced acid loads have been shown to increase renal endothelin-1 activity, and it is hypothesized that increased dietary acid-induced endothelin-1 activity may be a causative progression factor in human renal insufficiency and that this might be reversed by provision of dietary alkali. We sought to clarify, in normal human volunteers, the role of endothelin-1 in renal acidification and to determine whether the effect is dependent on dietary sodium chloride. Acid-base equilibrium was studied in seven normal human volunteers with experimentally induced metabolic acidosis [NH4Cl 2.1 mmol·kg body weight (BW)−1·day−1] with and without inhibition of endogenous endothelin-1 activity by the endothelin A/B-receptor antagonist bosentan (125 BID p.o./day) both during dietary NaCl restriction (20 mmol/day) and NaCl repletion (2 mmol NaCl·kg BW−1·day−1). During NaCl restriction, but not in the NaCl replete state, bosentan significantly increased renal net acid excretion in association with stimulation of ammoniagenesis resulting in a significantly increased plasma bicarbonate concentration (19.0 ± 0.8 to 20.1 ± 0.9 mmol/l) despite a decrease in mineralocorticoid activity and an increase in endogenous acid production. In pre-existing human metabolic acidosis, endothelin-1 activity worsens acidosis by decreasing the set-point for renal regulation of plasma bicarbonate concentration, but only when dietary NaCl provision is restricted.

Teaching acid/base physiology in the laboratory

2010 ◽  
Vol 34 (4) ◽  
pp. 233-238 ◽  
Author(s):  
Ulla G. Friis ◽  
Ronni Plovsing ◽  
Klaus Hansen ◽  
Bent G. Laursen ◽  
Birgitta Wallstedt
Keyword(s):  
Metabolic Acidosis ◽  
Medical Students ◽  
Respiratory Alkalosis ◽  
Theory And Practice ◽  
Single Group ◽  
Acid Base ◽  
Laboratory Exercise ◽  
Base Disorder

Acid/base homeostasis is one of the most difficult subdisciplines of physiology for medical students to master. A different approach, where theory and practice are linked, might help students develop a deeper understanding of acid/base homeostasis. We therefore set out to develop a laboratory exercise in acid/base physiology that would provide students with unambiguous and reproducible data that clearly would illustrate the theory in practice. The laboratory exercise was developed to include both metabolic acidosis and respiratory alkalosis. Data were collected from 56 groups of medical students that had participated in this laboratory exercise. The acquired data showed very consistent and solid findings after the development of both metabolic acidosis and respiratory alkalosis. All results were consistent with the appropriate diagnosis of the acid/base disorder. Not one single group failed to obtain data that were compatible with the diagnosis; it was only the degree of acidosis/alkalosis and compensation that varied.

scholarly journals Acid based disorders in intensive care unit: a hospital-based study

2019 ◽  
Vol 6 (1) ◽  
pp. 62 ◽  
Author(s):  
Babu Rajendran ◽  
Seetha Rami Reddy Mallampati ◽  
Sheju Jonathan Jha J.
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Metabolic Acidosis ◽  
Infectious Diseases ◽  
Respiratory Alkalosis ◽  
Simple Type ◽  
Acid Base ◽  
Icu Patients ◽  
Mixed Acid ◽  
Base Disorder

Background: Acid base disorders are common in the ICU patients and pose a great burden in the management of the underlying condition.Methods: Identifying the type of acid-base disorders in ICU patients using arterial blood gas analysis This was a retrospective case-controlled comparative study. 46 patients in intensive care unit of a reputed institution and comparing the type of acid-base disorder amongst infectious (10) and non-infectious (36) diseases.Results: Of the study population, 70% had mixed acid base disorders and 30% had simple type of acid base disorders. It was found that sepsis is associated with mixed type of acid-base disorders with most common being metabolic acidosis with respiratory alkalosis. Non-infectious diseases were mostly associated with metabolic alkalosis with respiratory acidosis. Analysis of individual acid base disorders revealed metabolic acidosis as the most common disturbance.Conclusions: These results projected the probability of acid bases disorders in various conditions and help in the efficient management. Mixed acid base disorders are the most common disturbances in the intensive care setup which is metabolic acidosis with respiratory alkalosis in infectious diseases and metabolic acidosis is the most common simple type of acid base disorder.

Ventilatory response to chronic metabolic acidosis and alkalosis in the dog

1984 ◽  
Vol 56 (6) ◽  
pp. 1640-1646 ◽  
Author(s):  
N. E. Madias ◽  
W. H. Bossert ◽  
H. J. Adrogue
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Ventilatory Response ◽  
Wide Spectrum ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Plasma Bicarbonate ◽  
Oral Sodium ◽  
Chronic Change

Systematic data are not available with regard to the anticipated appropriate responses of arterial PCO2 to primary alterations in plasma bicarbonate concentration. In the present study, we attempted to rigorously characterize the ventilatory response to chronic metabolic acid-base disturbances of graded severity in the dog. Animals with metabolic acidosis produced by prolonged HCl feeding and metabolic alkalosis of three different modes of generation, i.e., diuretics (ethacrynic acid or chlorothiazide), gastric drainage, and administration of deoxycorticosterone acetate (alone or in conjunction with oral sodium bicarbonate), were examined. The results indicate the existence of a significant and highly predictable ventilatory response to chronic metabolic acid-base disturbances. Moreover, the magnitude of the ventilatory response appears to be uniform throughout a wide spectrum of chronic metabolic acid-base disorders extending from severe metabolic acidosis to severe metabolic alkalosis; on average, arterial PCO2 is expected to change by 0.74 Torr for a 1-meq/l chronic change in plasma bicarbonate concentration of metabolic origin. Furthermore, the data suggest that the ventilatory response to chronic metabolic alkalosis is independent of the particular mode of generation.

Complex Acid-Base Disorders in Subacute Necrotizing Encephalomyelopathy (Leigh's Syndrome)

PEDIATRICS ◽  
1978 ◽  
Vol 61 (2) ◽  
pp. 278-281
Author(s):  
Gladys H. Hirschman ◽  
James C. M. Chan
Keyword(s):  
Metabolic Acidosis ◽  
Clinical Data ◽  
Renal Tubular Acidosis ◽  
Respiratory Alkalosis ◽  
Type I ◽  
Type Ii ◽  
Acid Base ◽  
Hybrid Type ◽  
Leigh’S Syndrome ◽  
Renal Tubular

This report describes a case of subacute necrotizing encephalomyelopathy (Leigh's syndrome) in a 7-month-old boy. The clinical data suggest an association with a disorder of renal tubular acidification, characterized by both (proximal) type II and (distal) type I renal tubular acidosis (hybrid type). Concomitantly, the initial uncompensated metabolic acidosis evolved into a mixed metabolic acidosis and respiratory alkalosis-features of this syndrome not previously reported.

The effects of respiratory alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo

1997 ◽  
Vol 273 (5) ◽  
pp. F698-F705
Author(s):  
R. Unwin ◽  
R. Stidwell ◽  
S. Taylor ◽  
G. Capasso
Keyword(s):  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Loop Of Henle ◽  
Transport Mechanisms ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Blood Ph ◽  
Tubule Lumen ◽  
Flux Formula

We have studied the effects of acute respiratory alkalosis (ARALK, hyperventilation) and acidosis (ARA, 8% CO2), chronic respiratory acidosis (CRA; 10% CO2 for 7–10 days), and subsequent recovery from CRA breathing air on loop of Henle (LOH) net bicarbonate flux ([Formula: see text]) by in vivo tubule microperfusion in anesthetized rats. In ARALK blood, pH increased to 7.6, and blood bicarbonate concentration ([[Formula: see text]]) decreased from 29 to 22 mM. Fractional urinary bicarbonate excretion ([Formula: see text]) increased threefold, but LOH[Formula: see text]was unchanged. In ARA, blood pH fell to 7.2, and blood [[Formula: see text]] rose from 28 to 34 mM; [Formula: see text] was reduced to <0.1%, but LOH[Formula: see text]was unaltered. In CRA, blood pH fell to 7.2, and blood [[Formula: see text]] increased to >50 mM, whereas[Formula: see text]decreased to <0.1%.[Formula: see text]was reduced by ∼30%. Bicarbonaturia occurred when CRA rats breathed air, yet LOH[Formula: see text]increased (by 30%) to normal. These results suggest that LOH[Formula: see text]is affected by the blood-to-tubule lumen [[Formula: see text]] gradient and[Formula: see text] backflux. When the usual perfusing solution at 20 nl/min was made[Formula: see text] free, mean[Formula: see text]was −34.5 ± 4.4 pmol/min compared with 210 ± 28.1 pmol/min plus [Formula: see text]. When a low-NaCl perfusate (to minimize net fluid absorption) containing mannitol and acetazolamide (2 × 10−4 M, to abolish H+-dependent[Formula: see text]) was used,[Formula: see text]was −112.8 ± 5.6 pmol/min. Comparable values for[Formula: see text]at 10 nl/min were −35.9 ± 5.8 and −72.5 ± 8.8 pmol/min, respectively. These data indicate significant backflux of[Formula: see text] along the LOH, which depends on the blood-to-lumen [[Formula: see text]] gradient; in addition to any underlying changes in active acid-base transport mechanisms, [Formula: see text]permeability and backflux are important determinants of LOH[Formula: see text]in vivo.

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