scholarly journals Can Venous Blood Gases Replace Arterial Blood Gases in Diabetic Ketoacidosis/Renal Failure Induced Metabolic Acidosis?

2015 ◽  
Vol 3 (3) ◽  
pp. 65-69
Author(s):  
Naveen Mohan ◽  
Gireesh Kumar K. P ◽  
Sreekrishnan T. P ◽  
Ajith Kumar J ◽  
Ajith V. ◽  
...  
2015 ◽  
Vol 35 (5) ◽  
pp. 873-881 ◽  
Author(s):  
Christopher K Willie ◽  
David B MacLeod ◽  
Kurt J Smith ◽  
Nia C Lewis ◽  
Glen E Foster ◽  
...  

The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO2 would affect cerebral metabolism more than hypoxia. PaO2 and PaCO2 were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial–jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO2-H+ relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO2 reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.


1965 ◽  
Vol 208 (4) ◽  
pp. 798-800 ◽  
Author(s):  
Hugo Chiodi ◽  
James W. Terman

Individual blood samples were collected anaerobically from the brachial arteries of adult White Rock hens and were analyzed for Po2, Pco2, pH, oxygen content and capacity, and CO2 content and capacity. A dissociation curve was constructed from data on equilibration of pooled venous blood. The average arterial oxygen saturation was 90%, the Pco2 was about 32 mm Hg, the Po2 was between 94 and 99 mm Hg, and the pH averaged 7.49. The dissociation curve, as has been shown before, was shifted to the right of most homeothermic species.


2019 ◽  
Vol 6 (4) ◽  
pp. 1016
Author(s):  
Sabiha Naz ◽  
Kiran Chugh ◽  
Isha Malik

Background: It is clearly mentioned in the medicine books that blood gas analysis from arterial puncture is the gold standard. But in the past few years it is commonly seen that clinicians have started trusting on venous blood gas analysis as well as started advising VBG (Venous blood gas) in the initial diagnosis of critical patients in emergency setting. Keeping this fact in mind, we designed a study to determine whether VBG could be a better replacement of ABG (Arterial blood gases) in the emergency where diverse pathological conditions are encountered.Methods: This prospective cross-sectional study comprised of 50 patients of 20-60 yrs age with a variety of diagnoses admitted in the emergency department. 50 paired samples (ABG+VBG) were obtained from them under strict aseptic precautions after obtaining their verbal consent. With a minimum delay of less than 2 min blood gas analysis was performed on blood gas analyzer. Parameters (pH, PCO2, PO2, HCO3, Base Excess and O2 saturation) from ABG and VBG were recorded and compared using Student’s Unpaired ‘t’ test.Results: pH and HCO3 showed statistical significant (p value <0.05) differences between ABG and VBG, while BE showed statistical non-significant (p value >0.05) difference between them. Contrary to this, PCO2, PO2 and O2 saturation from ABG and VBG showed statistical highly significant (p value <0.0001) differences.Conclusions: VBG should not be interchangeably considered in place of ABG with regard to pH, HCO3, PCO2, PO2 and O2 saturation in conditions where actual oxygenation status of patient is required (e.g.; hypovolemic shock, respiratory disorders, mechanically ventilated patients, etc.)


2000 ◽  
Vol 88 (5) ◽  
pp. 1715-1720 ◽  
Author(s):  
Paolo Palange ◽  
Silvia Forte ◽  
Paolo Onorati ◽  
Felice Manfredi ◽  
Pietro Serra ◽  
...  

To test the hypothesis that in chronic obstructive pulmonary disease (COPD) patients the ventilatory and metabolic requirements during cycling and walking exercise are different, paralleling the level of breathlessness, we studied nine patients with moderate to severe, stable COPD. Each subject underwent two exercise protocols: a 1-min incremental cycle ergometer exercise (C) and a “shuttle” walking test (W). Oxygen uptake (V˙o 2), CO2output (V˙co 2), minute ventilation (V˙e), and heart rate (HR) were measured with a portable telemetric system. Venous blood lactates were monitored. Measurements of arterial blood gases and pH were obtained in seven patients. Physiological dead space-tidal volume ratio (Vd/Vt) was computed. At peak exercise, W vs. CV˙o 2,V˙e, and HR values were similar, whereasV˙co 2 (848 ± 69 vs. 1,225 ± 45 ml/min; P < 0.001) and lactate (1.5 ± 0.2 vs. 4.1 ± 0.2 meq/l; P < 0.001) were lower, ΔV˙e/ΔV˙co 2(35.7 ± 1.7 vs. 25.9 ± 1.3; P < 0.001) and ΔHR/ΔV˙o 2values (51 ± 3 vs. 40 ± 4; P < 0.05) were significantly higher. Analyses of arterial blood gases at peak exercise revealed higher Vd/Vt and lower arterial partial pressure of oxygen values for W compared with C. In COPD, reduced walking capacity is associated with an excessively high ventilatory demand. Decreased pulmonary gas exchange efficiency and arterial hypoxemia are likely to be responsible for the observed findings.


1998 ◽  
Vol 274 (2) ◽  
pp. L301-L304 ◽  
Author(s):  
Yeong-Hau H. Lien ◽  
Li-Wen Lai

To investigate the role of carbonic anhydrase (CA) II on pulmonary CO2 exchange, we analyzed arterial blood gases from CA II-deficient and normal control mice. CA II-deficient mice had a low arterial blood pH (7.18 ± 0.06) and[Formula: see text] concentration ([[Formula: see text]]; 17.5 ± 1.9 meq/l) and a high [Formula: see text](47.4 ± 5.3 mmHg), consistent with mixed respiratory and metabolic acidosis. To eliminate the influence of metabolic acidosis on arterial blood gases, NaHCO3 (4 mmol/kg body weight) was given intraperitoneally, and arterial blood gases were analyzed 4 h later. Normal mice had a small increase in pH and were able to maintain [Formula: see text] and [[Formula: see text]]. The metabolic acidosis in CA II-deficient mice was corrected ([[Formula: see text]], 22.9 ± 2.4 meq/l), and respiratory acidosis became more profound ([Formula: see text], 50.4 ± 2.4 mmHg). These results indicate that CA II-deficient mice have a partial respiratory compensation for metabolic acidosis. We conclude that CA II-deficient mice have a mixed respiratory and metabolic acidosis. It is most likely that CO2 retention in these animals is due to CA II deficiency in both red blood cells and type II pneumocytes.


Sign in / Sign up

Export Citation Format

Share Document