The Respiratory Response to Chronic Metabolic Alkalosis and Acidosis in Disease

1973 ◽  
Vol 45 (4) ◽  
pp. 439-448 ◽  
Author(s):  
C. van Ypersele de Strihou ◽  
A. Frans
Keyword(s):  
Metabolic Alkalosis ◽  
Carbon Dioxide Tension ◽  
Individual Response ◽  
Chronic Haemodialysis ◽  
Confidence Limits ◽  
Respiratory Response ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Ph ◽  
The Individual

1. The respiratory response to chronic metabolic alkalosis was defined on the basis of 182 determinations of the arterial blood pH, Pco2, HCO3− concentration and Po2 obtained in thirty uraemic patients undergoing chronic haemodialysis. Plasma bicarbonate concentrations, [HCO3−], ranged from 20 to 38 mmol/l before dialysis, and were elevated by increasing the acetate content of the dialysate. 2. The calculated arterial carbon dioxide tension (Pa,co2) was linearly related to HCO3−, Pa,co2 reaching 50 mmHg at a [HCO3−] of 37.5 mmol/l. This response was virtually identical with that previously reported in chronic metabolic acidosis. The 95% confidence limits of the respiratory adaptation to chronic metabolic acid-base disorders were calculated for [HCO3−] ranging from 11 to 38 mmol/l. 3. Analysis of the individual response lines of thirteen patients revealed no difference among their slopes but significant differences among their elevations. Each subject appears thus to have his own threshold to acid-base stimuli. 4. Hypoxaemia developed with increasing [HCO3−], Pa,o2 falling in a curvilinear fashion to reach 70 mmHg at a [HCO3−] of 37.5 mmol/l.

ERRATA

PEDIATRICS ◽  
1980 ◽  
Vol 65 (5) ◽  
pp. 1006-1006
Keyword(s):  
Metabolic Acidosis ◽  
Diagnostic Approach ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Ph ◽  
P 351 ◽  
Normal Acid

In the article "A Diagnostic Approach to Metabolic Acidosis in Children" by Kappy and Morrow (Pediatrics 65:351-356, 1980) on p 351 under "Normal Acid-Base Physiology" the normal arterial blood pH is maintained at 7.40 (H+ = 39.8 nEq/liter not mEq/liter.

Acid-Base Regulation Following Exhaustive Exercise: A Comparison Between Freshwaterand Sea Water-Adapted Rainbow Trout (Salmo Gairdneri)

1989 ◽  
Vol 141 (1) ◽  
pp. 407-418 ◽  
Author(s):  
Y. TANG ◽  
D. G. McDONALD ◽  
R. G. BOUTILIER
Keyword(s):  
Rainbow Trout ◽  
Sea Water ◽  
Environmental Water ◽  
Exhaustive Exercise ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Genetic Stock ◽  
Arterial Blood ◽  
Blood Ph ◽  
Counter Ions

Blood acid-base regulation following exhaustive exercise was investigated in freshwater- (FW) and seawater- (SW) adapted rainbow trout (Salmo gairdneri) of the same genetic stock. Following exhaustive exercise at 10°C, both FW and SW trout displayed a mixed respiratory and metabolic blood acidosis. However, in FW trout the acidosis was about double that of SW trout and arterial blood pH took twice as long to correct. These SW/FW differences were related to the relative amounts of net H+ equivalent excretion to the environmental water, SW trout excreting five times as much as FW trout. The greater H+ equivalent excretion in SW trout may be secondary to changes in the gills that accompany the adaptation from FW to SW. It may also be related to the higher concentrations of HCO3− as well as other exchangeable counter-ions (Na+ and Cl−) in the external medium in SW compared to FW.

Cerebrospinal fluid in man native to high altitude

1964 ◽  
Vol 19 (2) ◽  
pp. 319-321 ◽  
Author(s):  
J. W. Severinghaus ◽  
A. Carceleń B.
Keyword(s):  
Cerebrospinal Fluid ◽  
High Altitude ◽  
Sea Level ◽  
Regulation Of Respiration ◽  
Acid Base ◽  
Peripheral Chemoreceptor ◽  
Arterial Blood ◽  
Blood Ph ◽  
The Difference

CSF pH was shown in a prior report to remain essentially constant during 8 days of acclimatization to 3,800 m. In order to further evaluate the possible role of CSF acid-base equilibria in the regulation of respiration, 20 Peruvian Andean natives were studied at altitudes of 3,720–4,820 m. In ten subjects at 3,720 m, means were: CSF pH 7.327, Pco2 43, HCO3- 21.5, Na+ 136, K+ 2.6, Cl- 124, lactate 30 mg/100 ml. Arterial blood: pH 7.43, Pco2 32.5, HCO3- 21.3, Na+ 136, K+ 4.2, Cl- 107, hematocrit 49, SaOO2 89.6. In six subjects at 4,545 m and four at 4,820 m CSF values were not significantly different; mean arterial Pco2 was 32.6 and 32.3, respectively. The only significant variations with altitude were the expected lowering of PaOO2 to 47 and 43.5 mm Hg, and of SaOO2 to 84.2 and 80.7, and increase of hematocrit to 67% and 75%, respectively. The natives differed from recently acclimatized sea-level residents in showing less ventilation (higher Pco2) in response to the existing hypoxia, and less alkaline arterial blood. The difference appears to relate to peripheral chemoreceptor response to hypoxia rather than central medullary chemoreceptor. respiratory regulation at high altitude; chronic acclimatization to altitude; peripheral chemoreceptor response to hypoxia; CSF and medullary respiratory chemoreceptors Submitted on June 12, 1963

The Impact of Peritonitis on Peritoneal and Systemic Acid-Base Status of Patients on Continuous Ambulatory Peritoneal Dialysis

1994 ◽  
Vol 14 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Jacques J. Sennesael ◽  
Godelieve C. De Smedt ◽  
Patricia Van der Niepen ◽  
Dierik L. Verbeelen
Keyword(s):  
Staphylococcus Aureus ◽  
Peritoneal Dialysis ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Acid Base ◽  
Gram Positive ◽  
Gram Negative ◽  
Arterial Blood ◽  
Blood Ph ◽  
Acid Base Status ◽  
And Staphylococcus Aureus

Objective To assess the possible effects of peritonitis on peritoneal and systemic acid-base status. Design pH, pCO2, lactate, and total leukocyte and differential count were simultaneously determined in the overnight dwell peritoneal dialysis effluent (PDE) and arterial blood in noninfected patients (controls) and on days 1, 3, and 5 from the onset of peritonitis. Setting University multidisciplinary dialysis program. Patients Prospective analysis of 63 peritonitis episodes occurring in 30 adult CAPD patients in a single center. Results In controls, mean (±SD) acid-base parameters were pH 7.41 ±0.05, pCO2 43.5±2.6 mm Hg, lactate 2.5±1.5 mmol/L in the PDE, and pH 7.43±0.04, PaCO2 36.8±3.8 mm Hg, lactate 1.4±0.7 mmol/L in the blood. In sterile (n=6), gram-positive (n=34), and Staphylococcus aureus (n=9) peritonitis PDE pH's on day 1 were, respectively, 7. 29±0.07, 7. 32±0.07, and 7.30±0.08 (p<0.05 vs control). In gram -negative peritonitis (n=14) PDE pH was 7.21 ±0.08 (p<0.05 vs all other groups). A two-to-threefold increase in PDE lactate was observed in all peritonitis groups, but a rise in pCO2 was only seen in gram -negative peritonitis. Acid-base profile of PDE had returned to control values by day 3 in sterile, gram -positive and Staphylococcus aureus peritonitis and by day 5 in gramnegative peritonitis. Despite a slight increase in plasma lactate on the first day of peritonitis, arterial blood pH was not affected by peritonitis. Conclusion PDE pH is decreased in continuous ambulatory peritoneal dialysis (CAPD) peritonitis, even in the absence of bacterial growth. In gram-negative peritonitis, PDE acidosis is more pronounced and prolonged, and pCO2 is markedly increased. Arterial blood pH is not affected by peritonitis.

Hyperoxia of cerebral venous blood and cisternal cerebrospinal fluid following arterial air embolism

1972 ◽  
Vol 37 (1) ◽  
pp. 30-35 ◽  
Author(s):  
Norval M. Simms ◽  
Don M. Long ◽  
James H. Matthews ◽  
Shelley N. Chou
Keyword(s):  
Cerebrospinal Fluid ◽  
Oxygen Tension ◽  
Venous Blood ◽  
Air Embolism ◽  
Carbon Dioxide Tension ◽  
Acid Base ◽  
Content Type ◽  
Arterial Blood ◽  
Base Parameters ◽  
The Right

✓ Oxygen tension and acid-base parameters of cerebral venous blood and cisternal cerebrospinal fluid, as well of femoral arterial blood, were studied in 14 dogs following injection of varying amounts of room air into the right vertebral artery. Acute elevations in oxygen tension were demonstrated in both cerebral venous blood and CSF, whereas hypoxemia occurred concomitantly in systemic arterial blood. Post-embolic increases in carbon dioxide tension with reciprocal diminutions in pH were evident in all sampling sites. The pathophysiological bases for these air-induced alterations are discussed.

scholarly journals Isoflurane-induced acidosis depresses basal and PGE2-stimulated duodenal bicarbonate secretion in mice

2007 ◽  
Vol 292 (3) ◽  
pp. G899-G904 ◽  
Author(s):  
Markus Sjöblom ◽  
Olof Nylander
Keyword(s):  
Base Excess ◽  
Ringer Solution ◽  
Bicarbonate Secretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
In Vivo Experiments ◽  
Arterial Blood ◽  
Blood Ph ◽  
Base Balance

When running in vivo experiments, it is imperative to keep arterial blood pressure and acid-base parameters within the normal physiological range. The aim of this investigation was to explore the consequences of anesthesia-induced acidosis on basal and PGE2-stimulated duodenal bicarbonate secretion. Mice (strain C57bl/6J) were kept anesthetized by a spontaneous inhalation of isoflurane. Mean arterial blood pressure (MAP), arterial acid-base balance, and duodenal mucosal bicarbonate secretion (DMBS) were studied. Two intra-arterial fluid support strategies were used: a standard Ringer solution and an isotonic Na2CO3 solution. Duodenal single perfusion was used, and DMBS was assessed by back titration of the effluent. PGE2 was used to stimulate DMBS. In Ringer solution-infused mice, isoflurane-induced acidosis became worse with time. The blood pH was 7.15–7.21 and the base excess was about −8 mM at the end of experiments. The continuous infusion of Na2CO3 solution completely compensated for the acidosis. The blood pH was 7.36–7.37 and base excess was about 1 mM at the end of the experiment. Basal and PGE2-stimulated DMBS were markedly greater in animals treated with Na2CO3 solution than in those treated with Ringer solution. MAP was slightly higher after Na2CO3 solution infusion than after Ringer solution infusion. We concluded that isoflurane-induced acidosis markedly depresses basal and PGE2-stimulated DMBS as well as the responsiveness to PGE2, effects prevented by a continuous infusion of Na2CO3. When performing in vivo experiments in isoflurane-anesthetized mice, it is recommended to supplement with a Na2CO3 infusion to maintain a normal acid-base balance.

The Ventilatory Response in Severe Metabolic Acidosis

1976 ◽  
Vol 50 (5) ◽  
pp. 367-373 ◽  
Author(s):  
M. Fulop
Keyword(s):  
Metabolic Acidosis ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Carbon Dioxide Tension ◽  
Pulmonary Insufficiency ◽  
Plasma Lactate ◽  
Severe Metabolic Acidosis ◽  
Arterial Blood ◽  
Blood Ph ◽  
Insufficient Time

1. The ventilatory response to severe metabolic acidosis was studied by measuring arterial blood carbon dioxide tension and pH in sixty-seven patients with blood pH < 7·10, none of whom had hypercapnia, pulmonary oedema, or chronic pulmonary insufficiency. The results were compared with those previously found in patients with uncomplicated diabetic ketoacidosis. 2. By that comparison, fifty-two of the sixty-seven patients with blood pH < 7·10 were judged to have ‘appropriate hypocapnia’, and fifteen had ‘submaximal hypocapnia’. Thirteen of the latter fifteen had circulatory failure and/or acute hypoxia, and seven of nine in whom it was measured had plasma lactate >9 mmol/l. 3. Hyperventilation was therefore usually well sustained in these patients with severe metabolic acidosis, except in most of those with acute tissue hypoxia. The latter may have had insufficient time to achieve maximum hyperventilation in response to their acidosis, or perhaps their submaximal hypercapnia presaged imminent failure of the hyperventilatory response.

Bicarbonate reabsorption by the kidney of the newborn rabbit

1989 ◽  
Vol 256 (1) ◽  
pp. F29-F34
Author(s):  
A. J. van der Heijden ◽  
J. P. Guignard
Keyword(s):  
Metabolic Alkalosis ◽  
Filtration Rate ◽  
Animal Species ◽  
Carbon Dioxide Tension ◽  
Acid Base ◽  
Renal Handling ◽  
Newborn Rabbit ◽  
Bicarbonate Reabsorption ◽  
Filtered Load ◽  
Reabsorption Rate

Bicarbonate reabsorption by the immature kidney in response to acute acid-base changes was assessed in 50 anesthetized newborn rabbits before the end of nephrogenesis. The normal newborn rabbit (age 5-12 days) is in a state of hypochloremic metabolic alkalosis (PHCO3-, 31.9 +/- 0.6 mmol/l; PCl-, 83.1 +/- 1.0) and excretes a hypertonic (Uosmol = 578 +/- 41 mosmol/kgH2O), alkaline (UpH = 7.40 +/- 0.15) urine containing 50 +/- 9 mmol/l Cl- and 13 +/- 4 mmol/l Na+. The alkalosis is probably generated by an alkaline load contained in the mother's milk and maintained by a state of chloride wasting and volume contraction. In this alkalotic model, bicarbonate reabsorption, expressed per milliliter glomerular filtration rate (GFR), correlates positively with arterial CO2 pressure (PaCO2). The ability of the immature kidney to reclaim filtered bicarbonate in response to an elevation of the plasma carbon dioxide tension remains unlimited up to PaCO2 of 110 mmHg (y = 20.7 + 0.15 x, r = 0.82, P less than 0.001). Hypercapnia is associated with a marked fall in GFR, so that the positive correlation between bicarbonate reabsorption and PaCO2 vanishes when the bicarbonate reabsorption rate is expressed in absolute terms. Bicarbonate reabsorption is strongly dependent on the filtered load during both acutely induced metabolic acidosis and alkalosis. The acid-base state of the newborn rabbit is in sharp contrast with that of most animal species, and the renal handling of bicarbonate as a function of GFR does not show signs of tubular immaturity.

Acid-Base Relationships in the Blood of the Toad, Bufo Marinus: III. The Effects of Burrowing

1979 ◽  
Vol 82 (1) ◽  
pp. 357-365
Author(s):  
R. G. BOUTILIER ◽  
D. J. RANDALL ◽  
G. SHELTON ◽  
D. P. TOEWS
Keyword(s):  
Respiratory Acidosis ◽  
Lung Ventilation ◽  
Progressive Increase ◽  
Bufo Marinus ◽  
Sharp Decline ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Ph ◽  
Equilibrium Ratio ◽  
Toad Bufo

When Bufo marinus burrows, the skin becomes intimately surrounded by substrate but the nares always remain exposed to the surface air. Upon entering into a state of dormancy the animal hypoventilates and this together with the loss of the skin as a respiratory site results in a rise in arterial blood Pcoco2 despite a probable decline in metabolism. Even though lung ventilation falls, the toad regulates blood pH and the respiratory acidosis is progressively compensated for by a progressive increase in plasma [HCO3-] along the course of an elevated PCOCO2 isopleth. At steady state, the acidosis is fully compensated for by a new equilibrium ratio of HCO3- to PCOCO2 at the same pH as the non-burrowed animal. Arousal from the dormant state at this time results in a marked lung hyperventilation and a sharp decline in body CO2 stores

Sign in / Sign up

Export Citation Format

Share Document