scholarly journals Is venous blood a more reliable description of acid-base state following simulated hypo- and hyperventilation?

2021 ◽  
Vol 29 (1) ◽  
Author(s):  
Lisha Shastri ◽  
Søren Kjærgaard ◽  
Peter S. Thyrrestrup ◽  
Stephen E. Rees ◽  
Lars P. Thomsen
Keyword(s):  
Repeated Measures ◽  
Elective Surgery ◽  
Venous Blood ◽  
Reference Method ◽  
Breath Holding ◽  
Metabolic Disturbances ◽  
Acid Base ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Acute Changes

Abstract Background ABGs are performed in acute conditions as the reference method for assessing the acid-base status of blood. Hyperventilation and breath-holding are common ventilatory changes that occur around the time of sampling, rapidly altering the ‘true’ status of the blood. This is particularly relevant in emergency medicine patients without permanent arterial catheters, where the pain and anxiety of arterial punctures can cause ventilatory changes. This study aimed to determine whether peripheral venous values could be a more reliable measure of blood gases following acute changes in ventilation. Methods To allow for characterisation of ventilatory changes typical of acutely ill patients, but without the confounding influence of perfusion or metabolic disturbances, 30 patients scheduled for elective surgery were studied in a prospective observational study. Following anaesthesia, and before the start of the surgery, ventilator settings were altered to achieve a + 100% or − 60% change in alveolar ventilation (‘hyper-’ or ‘hypoventilation’), changes consistent with the anticipation of a painful arterial puncture commonly encountered in the emergency room. Blood samples were drawn simultaneously from indwelling arterial and peripheral venous catheters at baseline, and at 15, 30, 45, 60, 90 and 120 s following the ventilatory change. Comparisons between the timed arterial (or venous) samples were done using repeated-measures ANOVA, with post-hoc analysis using Bonferroni’s correction. Results Arterial blood pH and PCO2 changed rapidly within the first 15–30s after both hyper- and hypoventilation, plateauing at around 60s (∆pH = ±0.036 and ∆PCO2 = ±0.64 kPa (4.7 mmHg), respectively), with peripheral venous values remaining relatively constant until 60s, and changing minimally thereafter. Mean arterial changes were significantly different at 30s (P < 0.001) when compared to baseline, in response to both hyper- and hypoventilation. Conclusion This study has shown that substantial differences in arterial and peripheral venous acid-base status can be due to acute changes in ventilation, commonly seen in the ER over the 30s necessary to sample arterial blood. If changes are transient, peripheral venous blood may provide a more reliable description of acid-base status.

Breath holding during intense exercise: arterial blood gases, pH, and lactate

1988 ◽  
Vol 64 (5) ◽  
pp. 1947-1952 ◽  
Author(s):  
G. O. Matheson ◽  
D. C. McKenzie
Keyword(s):  
Repeated Measures ◽  
Intermittent Exercise ◽  
Blood Gases ◽  
Breath Holding ◽  
Arterial Blood Gases ◽  
Acid Base ◽  
Arterial Blood ◽  
Repeated Measures Analysis ◽  
Acid Base Status ◽  
Arterial Po2

Seven healthy endurance-trained [maximal O2 uptake (VO2max) = 57.1 +/- 4.1 ml.kg-1.min-1)] female volunteers (mean age 24.4 +/- 3.6 yr) served as subjects in an experiment measuring arterial blood gases, acid-base status, and lactate changes while breath holding (BH) during intense intermittent exercise. By the use of a counterbalance design, each subject repeated five intervals of a 15-s on:30-s off treadmill run at 125% VO2max while BH and while breathing freely (NBH). Arterial blood for pH, PO2, PCO2, O2 saturation (SO2) HCO3, and lactate was sampled from a radial arterial catheter at the end of each work and rest interval and throughout recovery, and the results were analyzed using repeated-measures analysis of variance. Significant reductions in pHa (delta mean = 0.07, P less than 0.01), arterial PO2 (delta mean = 24.2 Torr, P less than 0.01), and O2 saturation (delta mean = 4.6%, P less than 0.01) and elevations in arterial PCO2 (delta mean = 8.2 Torr, P less than 0.01) and arterial HCO3 (delta mean = 1.3 meq/l, P = 0.05) were found at the end of each exercise interval in the BH condition. All of the observed changes in arterial blood gases and acid-base status induced by BH were reversed during the rest intervals. During recovery, significantly (P less than 0.025) greater levels of arterial lactate were found in the BH condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Relative effects of carbonic anhydrase infusion or inhibition on carbon dioxide transport and acid-base status in the sea lamprey Petromyzon marinus following exercise

1996 ◽  
Vol 199 (4) ◽  
pp. 933-940
Author(s):  
B Tufts ◽  
S Currie ◽  
J Kieffer
Keyword(s):  
Carbon Dioxide ◽  
Carbonic Anhydrase ◽  
Venous Blood ◽  
Extracellular Fluid ◽  
Respiratory Acidosis ◽  
Acid Base ◽  
Carbon Dioxide Transport ◽  
Co2 Transport ◽  
Arterial Blood ◽  
Acid Base Status

In vivo experiments were carried out to determine the relative effects of carbonic anhydrase (CA) infusion or inhibition on carbon dioxide (CO2) transport and acid-base status in the arterial and venous blood of sea lampreys recovering from exhaustive exercise. Infusion of CA into the extracellular fluid did not significantly affect CO2 transport or acid-base status in exercised lampreys. In contrast, infusion of the CA inhibitor acetazolamide resulted in a respiratory acidosis in the blood of recovering lampreys. In acetazolamide-treated lampreys, the post-exercise extracellular pH (pHe) of arterial blood was significantly lower than that in the saline-infused (control) lampreys. The calculated arterial and venous partial pressure of carbon dioxide (PCO2) and the total CO2 concentration in whole blood (CCO2wb) and red blood cells (CCO2rbc) during recovery in the acetazolamide-infused lampreys were also significantly greater than those values in the saline-infused control lampreys. These results suggest that the CO2 reactions in the extracellular compartment of lampreys may already be in equilibrium and that the access of plasma bicarbonate to CA is probably not the sole factor limiting CO2 transport in these animals. Furthermore, endogenous red blood cell CA clearly has an important role in CO2 transport in exercising lampreys.

Assessing Acid–Base Status in Circulatory Failure: Relationship Between Arterial and Peripheral Venous Blood Gas Measurements in Hypovolemic Shock

2018 ◽  
Vol 35 (5) ◽  
pp. 511-518
Author(s):  
Scott E. Rudkin ◽  
Craig L. Anderson ◽  
Tristan R. Grogan ◽  
David A. Elashoff ◽  
Richard M. Treger
Keyword(s):  
Venous Blood ◽  
Hypovolemic Shock ◽  
Circulatory Failure ◽  
Blood Gas ◽  
Central Venous ◽  
Acid Base ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Venous Blood Gas ◽  
The Relationship

Background and Objectives: In severe circulatory failure agreement between arterial and mixed venous or central venous values is poor; venous values are more reflective of tissue acid–base imbalance. No prior study has examined the relationship between peripheral venous blood gas (VBG) values and arterial blood gas (ABG) values in hemodynamic compromise. The objective of this study was to examine the correlation between hemodynamic parameters, specifically systolic blood pressure (SBP) and the arterial–peripheral venous (A-PV) difference for all commonly used acid–base parameters (pH, Pco 2, and bicarbonate). Design, Setting, Participants, and Measurements: Data were obtained prospectively from adult patients with trauma. When an ABG was obtained for clinical purposes, a VBG was drawn as soon as possible. Patients were excluded if the ABG and VBG were drawn >10 minutes apart. Results: The correlations between A-PV pH, A-PV Pco 2, and A-PV bicarbonate and SBP were not statistically significant ( P = .55, .17, and .09, respectively). Although patients with hypotension had a lower mean arterial and peripheral venous pH and bicarbonate compared to hemodynamically stable patients, mean A-PV differences for pH and Pco 2 were not statistically different ( P = .24 and .16, respectively) between hypotensive and normotensive groups. Conclusions: In hypovolemic shock, the peripheral VBG does not demonstrate a higher CO2 concentration and lower pH compared to arterial blood. Therefore, the peripheral VBG is not a surrogate for the tissue acid–base status in hypovolemic shock, likely due to peripheral vasoconstriction and central shunting of blood to essential organs. This contrasts with the selective venous respiratory acidosis previously demonstrated in central venous and mixed venous measurements in circulatory failure, which is more reflective of acid–base imbalance at the tissue level than arterial blood. Further work needs to be done to better define the relationship between ABG and both central and peripheral VBG values in various types of shock.

scholarly journals Correlation of arterial blood gas measurement with peripheral venous blood gas values in adults patients admitted in ICU

2017 ◽  
Vol 5 (3) ◽  
pp. 11-17
Author(s):  
S Adhikari ◽  
S K Shrestha ◽  
B Srivastava ◽  
N B KC ◽  
B B Singh ◽  
...  
Keyword(s):  
Venous Blood ◽  
Gas Analysis ◽  
Care Practice ◽  
Blood Gas ◽  
Acid Base ◽  
Arterial Blood Gas ◽  
Peripheral Venous Blood ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Venous Blood Gas

Arterial blood gas (ABG) sampling is an essential investigation for assessment of acid-base status, oxygenation and ventilation in critical care practice. Arterial puncture to obtain arterial blood is more invasive procedure than venous and has more potential complications. To find out the correlation between arterial and peripheral venous blood gas values for pH, PCO2 and bicarbonate. Patients admitted in ICU requiring arterial blood gas analysis to determine their acid-base status or ventilatory status was included in the study. One milliliter of venous blood was obtained in a heparin flushed syringe within 5 minutes of getting arterial blood sample. Both labeled samples were processed immediately. Data were analyzed by student’s t-test. A total of 50 paired samples from 36 patients were evaluated. The mean differences between arterial and venous blood gas values for pH, PCO2 and bicarbonate were 0.02 units, -2.37 mmHg and -0.45 mEq/L respectively. Similarly, the correlation coefficients between arterial and venous parameters were 0.964, 0.881 and 0.906 for pH, PCO2 and bicarbonate respectively, which were statistically significant (p<0.001). Venous pH, PCO2 and bicarbonate showed a very high level of correlation with the respective arterial values.

Influence of changes in cardiac output on the acid-base status of arterial and mixed venous blood

1987 ◽  
Vol 410 (3) ◽  
pp. 257-262 ◽  
Author(s):  
Y. L. Hoogeveen ◽  
J. P. Zock ◽  
P. Rispens ◽  
W. G. Zijlstra
Keyword(s):  
Cardiac Output ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
Acid Base ◽  
Acid Base Status ◽  
Mixed Venous

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

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.

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.

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