Comparison of Carbon Dioxide Tension, PH and Standard Bicarbonate in Capillary Blood and in Arterial Blood with Special Respect to Relations in Patients with Impaired Cardiovascular and Pulmonary Function and During Exercise

1965 ◽  
Vol 17 (3) ◽  
pp. 223-229 ◽  
Author(s):  
G. Koch
Perfusion ◽  
2006 ◽  
Vol 21 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Frode Kristiansen ◽  
Jan Olav Høgetveit ◽  
Thore H Pedersen

This paper presents the clinical testing of a new capno-graph designed to measure the carbon dioxide tension at the oxygenator exhaust outlet in cardiopulmonary bypass (CPB). During CPB, there is a need for reliable, accurate and instant estimates of the arterial blood CO2 tension (PaCO2) in the patient. Currently, the standard practice for measuring PaCO2 involves the manual collection of intermittent blood samples, followed by a separate analysis performed by a blood gas analyser. Probes for inline blood gas measurement exist, but they are expensive and, thus, unsuitable for routine use. A well-known method is to measure PexCO2, ie, the partial pressure of CO2 in the exhaust gas output from the oxygenator and use this as an indirect estimate for PaCO2. Based on a commercially available CO2 sensor circuit board, a laminar flow capnograph was developed. A standard sample line with integrated water trap was connected to the oxygenator exhaust port. Fifty patients were divided into six different groups with respect to oxygenator type and temperature range. Both arterial and venous blood gas samples were drawn from the CPB circuit at various temperatures. Alfa-stat corrected pCO2 values were obtained by running a linear regression for each group based on the arterial temperature and then correcting the PexCO2 accordingly. The accuracy of the six groups was found to be (±SD): ±4.3, ±4.8, ±5.7, ±1.0, ±3.7 and ±2.1%. These results suggest that oxygenator exhaust capnography is a simple, inexpensive and reliable method of estimating the PaCO2 in both adult and pediatric patients at all relevant temperatures.


Author(s):  
John W. Kreit

Gas Exchange explains how four processes—delivery of oxygen, excretion of carbon dioxide, matching of ventilation and perfusion, and diffusion—allow the respiratory system to maintain normal partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) in the arterial blood. Partial pressure is important because O2 and CO2 molecules diffuse between alveolar gas and pulmonary capillary blood and between systemic capillary blood and the tissues along their partial pressure gradients, and diffusion continues until the partial pressures are equal. Ventilation is an essential part of gas exchange because it delivers O2, eliminates CO2, and determines ventilation–perfusion ratios. This chapter also explains how and why abnormalities in each of these processes may reduce PaO2, increase PaCO2, or both.


2016 ◽  
Vol 1 (60) ◽  
pp. 34-38
Author(s):  
Горячева ◽  
Svetlana Goryacheva ◽  
Приходько ◽  
Olga Prikhodko ◽  
Кострова ◽  
...  

Chronobiological aspects of blood gas composition in 24 patients with COPD were studied. To achieve this goal, the gas composition of the arterialized capillary blood simultaneously with the investigation of respiratory function was studied with an interval of 6 hours over 2 days. In healthy individuals and patients with mild COPD two types of gas composition of blood biorhythm – daytime and nighttime – were found. In patients with moderate, severe and very severe disease 3 types of biorhythm of partial oxygen and carbon dioxide tension – morning time, noontime and evening time were registered. In healthy individuals and patients with mild COPD gas composition of blood was characterized by significant degrees of freedom in relation to functioning of the respiratory system, which indicated the stored processes of adaptation to changing conditions of the external and internal environment. In patients with moderate, severe and very severe COPD at the moment of acrophase of circadian rhythm of lung function maximum partial oxygen pressure in the arterialized capillary blood was observed. During the batiphaze of circadian rhythm of the respiratory system the highest values of the partial carbon dioxide tension were revealed. Thus, it was found out that with the growth of the severity of the disease in patients with COPD abnormal rhythms of blood gas composition are registered; the dependence of circadian rhythm of blood gas composition on the functioning of the respiratory apparatus increases.


1992 ◽  
Vol 12 (6) ◽  
pp. 947-953 ◽  
Author(s):  
Qiong Wang ◽  
Olaf B. Paulson ◽  
Niels A. Lassen

The importance of nitric oxide (NO) for CBF variations associated with arterial carbon dioxide changes was investigated in halothane-anesthetized rats by using an inhibitor of nitric oxide synthase, NG-nitro-l-arginine (NOLAG). CBF was measured by intracarotid injection of 133Xe. In normocapnia, intracarotid infusion of 1.5, or 7.5, or 30 mg/kg NOLAG induced a dose-dependent increase of arterial blood pressure and a decrease of normocapnic CBF from 85 ± 10 to 78 ± 6, 64 ± 5, and 52 ± 5 ml 100g−1 min−1, respectively. This effect lasted for at least 2 h. Raising Paco2 from a control level of 40 to 68 mm Hg increased CBF to 230 ± 27 ml 100g−1 min−1, corresponding to a percentage CBF response (CO2 reactivity) of 3.7 ± 0.6%/mm Hg Paco2 in saline-treated rats. NOLAG attenuated this reactivity by 32, 49, and 51% at the three-dose levels. Hypercapnia combined with angiotensin to raise blood pressure to the same level as the highest dose of NOLAG did not affect the CBF response to hypercapnia. l-Arginine significantly prevented the effect of NOLAG on normocapnic CBF as well as blood pressure and also abolished its inhibitory effect on hypercapnic CBF. d-Arginine had no such effect. Decreasing Paco2 to 20 mm Hg reduced control CBF to 46 ± 3 ml 100g−1 min−1 with no further reduction after NOLAG. Furthermore, NOLAG did not change the percentage CBF response to an extracellular acidosis induced by acetazolamide (50 mg/kg). The results suggest that NO or a closely related compound is involved in the regulation of CBF in normocapnia and even more so in hypercapnia.


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