Contribution of Acid-Base Changes to Control of Breathing During Exercise

The mechanisms mediating the exercise hyperpnea remain controversial; there is no unequivocal evidence that any of numerous proposed mechanisms mediates the hyperpnea. However, a great deal has been learned including the potential role of changes in PCO2, [H+], strong ion differences (SID), weak acids, or any other acid-base component. The contribution of acid-base changes to the hyperpnea during exercise is likely through known or postulated chemoreceptors. Two of these, pulmonary and intracranial chemoreceptors, do not appear critical for the ventilatory adjustments to meet the metabolic demands of exercise. A third, the carotid chemoreceptors, appear to fine-tune alveolar ventilation during exercise to minimize disruptions in arterial blood gases. The role of the fourth chemoreceptors, those within skeletal muscles, is least clear. However, there is evidence that they do contribute to the hyperpnea, and it is quite clear that a muscle chemoreflex contributes to the exercise muscle pressor reflex; thus the contribution of these chemoreceptors to the exercise hyperpnea requires additional study. Key words: ventilation, hydrogen ion, PaCO2, PO2

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DIGITALIS TOLERANCE IN YOUNG PUPPIES

PEDIATRICS ◽

10.1542/peds.46.5.730 ◽

1970 ◽

Vol 46 (5) ◽

pp. 730-736

Author(s):

Katherine H. Halloran ◽

Steven C. Schimpff ◽

Jean G. Nicolas ◽

Norman S. Talner

Keyword(s):

Blood Gases ◽

Acid Base Balance ◽

Acid Base ◽

Littermate Control ◽

Premature Ventricular Contractions ◽

Toxic Dose ◽

Arterial Blood ◽

Wide Range ◽

Base Balance ◽

The Mean

Tolerance to acetyl strophanthidin, a rapid-acting cardiac aglycone, was determined in 28 anesthetized mongrel puppies, ages 16 to 56 days, and compared to tolerance in 16 littermate puppies in whom acute hypercapnic acidemia was produced. The tolerance was also compared to that of four adult mongrel dogs. The toxic dose was defined as the intravenous amount required to produce four consecutive premature ventricular contractions. A marked variation in the toxic dose was found in the 28 control puppies (range 83 to 353 µg/kg, mean 169 µg/kg) which could not be correlated with age, arterial blood gases or pH, serum potassium or sodium, arterial pressure, or heart rate. The toxic dose was significantly greater in the puppies than in the adult dogs, in whom the mean toxic dose was 64 µg/kg (range 50 to 89 µg/kg). A significant increase in tolerance was also observed in the puppies with hypercapnic acidemia (mean toxic dose 220 µg/kg, range 93 to 375 µg/kg) in comparison to tolerance in the control puppies and despite the wide range of tolerance, each of the puppies with hypercapnic acidemia showed greater tolerance than its littermate control puppy. Assessment of the clinical implications of these findings will require study of the effects of alterations in acid-base balance on the inotropic effect of acetyl strophanthidin in addition to the toxic electrophysiologic effects.

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Role of tracheal and bronchial circulation in respiratory heat exchange

Journal of Applied Physiology ◽

10.1152/jappl.1985.58.1.217 ◽

1985 ◽

Vol 58 (1) ◽

pp. 217-222 ◽

Cited By ~ 50

Author(s):

E. M. Baile ◽

R. W. Dahlby ◽

B. R. Wiggs ◽

P. D. Pare

Keyword(s):

Blood Flow ◽

Blood Gases ◽

Lung Parenchyma ◽

Arterial Blood ◽

Respiratory Heat Loss ◽

Reference Flow ◽

Pulmonary Arterial ◽

End Tidal ◽

Humidified Air

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.

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Hyperlactacemia in critically ill children: comparison of traditional and Fencl-Stewart methods

Paediatrica Indonesiana ◽

10.14238/pi47.1.2007.35-41 ◽

2007 ◽

Vol 47 (1) ◽

pp. 35

Author(s):

Hari Kushartono ◽

Antonius H. Pudjiadi ◽

Susetyo Harry Purwanto ◽

Imral Chair ◽

Darlan Darwis ◽

...

Keyword(s):

Base Excess ◽

Pediatric Intensive Care ◽

Blood Gases ◽

Critically Ill Children ◽

Strongly Correlated ◽

Acid Base ◽

Arterial Blood ◽

Acid Base Status ◽

Lactate Levels ◽

Elevated Lactate

Background Base excess is a single variable used to quantifymetabolic component of acid base status. Several researches havecombined the traditional base excess method with the Stewartmethod for acid base physiology called as Fencl-Stewart method.Objective The purpose of the study was to compare two differentmethods in identifying hyperlactacemia in pediatric patients withcritical illness.Methods The study was performed on 43 patients admitted tothe pediatric intensive care unit of Cipto MangunkusumoHospital, Jakarta. Sodium, potassium, chloride, albumin, lactateand arterial blood gases were measured. All samples were takenfrom artery of all patients. Lactate level of >2 mEq/L was definedas abnormal. Standard base excess (SBE) was calculated fromthe standard bicarbonate derived from Henderson-Hasselbalchequation and reported on the blood gas analyzer. Base excessunmeasured anions (BE UA ) was calculated using the Fencl-Stewartmethod simplified by Story (2003). Correlation between lactatelevels in traditional and Fencl-Stewart methods were measuredby Pearson’s correlation coefficient .Results Elevated lactate levels were found in 24 (55.8%) patients.Lactate levels was more strongly correlated with BE UA (r = - 0.742,P<0.01) than with SBE (r = - 0.516, P<0.01).Conclusion Fencl-Stewart method is better than traditionalmethod in identifying patients with elevated lactate levels, so theFencl-Stewart method is suggested to use in clinical practice.

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Introduction to Acid-Base Chemistry and Arterial Blood Gases

Pathophysiologic Basis of Acid-Base Disorders ◽

10.1007/978-981-16-0526-0_5 ◽

2021 ◽

pp. 71-82

Author(s):

Farrokh Habibzadeh ◽

Mahboobeh Yadollahie ◽

Parham Habibzadeh

Keyword(s):

Blood Gases ◽

Arterial Blood Gases ◽

Acid Base ◽

Arterial Blood

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VALIDITY OF ARTERIAL BLOOD GASES AND ACID-BASE STATUS OBTAINED BY VARIOUS INDIRECT METHODS

Medicine & Science in Sports & Exercise ◽

10.1249/00005768-197100310-00050 ◽

1971 ◽

Vol 3 (1) ◽

pp. l

Author(s):

Hubert Forster

Keyword(s):

Blood Gases ◽

Arterial Blood Gases ◽

Acid Base ◽

Indirect Methods ◽

Arterial Blood ◽

Acid Base Status

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Cerebrospinal fluid in man native to high altitude

Journal of Applied Physiology ◽

10.1152/jappl.1964.19.2.319 ◽

1964 ◽

Vol 19 (2) ◽

pp. 319-321 ◽

Cited By ~ 28

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

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

Journal of Applied Physiology ◽

10.1152/jappl.1989.66.6.2895 ◽

1989 ◽

Vol 66 (6) ◽

pp. 2895-2900 ◽

Cited By ~ 8

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.

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