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.

Acid-base changes in blood and cerebrospinal fluid during altered ventilation

1961 ◽  
Vol 16 (6) ◽  
pp. 1016-1018 ◽  
Author(s):  
C. R. Merwarth ◽  
H. O. Sieker
Keyword(s):  
Carbon Dioxide ◽  
Cerebrospinal Fluid ◽  
Venous Blood ◽  
Clinical Importance ◽  
Carbon Dioxide Tension ◽  
Acid Base ◽  
Sagittal Sinus ◽  
Arterial Blood ◽  
Arterial Ph ◽  
The Central Nervous System

Functional abnormalities of the central nervous system are observed with hypo- and hyperventilation. This study correlates changes of pH, carbon dioxide tension and carbon dioxide content in arterial and cerebral venous blood and cerebrospinal fluid during altered ventilation. With the experimental design in which ventilation was controlled and the sagittal sinus, femoral artery, and cisterna magna were cannulated, a slight metabolic acidosis was found. With 10% CO2 inhalation acidosis occurred in both blood and spinal fluid and early in the period of inhalation, the usual cerebrospinal-arterial fluid pCO2 gradient was reversed. With hyperventilation, pH and pCO2 changes were more pronounced in the arterial blood but, as hyperventilation was continued, the arterial-cerebrospinal fluid difference decreased. It appeared likely that brain tissue acts as an important buffer, absorbing and releasing CO2 during states of altered ventilation. CO2 diffuses rapidly across cell boundaries, whereas bicarbonate crosses more slowly, thus providing an explanation for the differences noted between blood and cerebrospinal fluid. The particular clinical importance of these observations is that arterial pH, pCO2, and CO2 content may not accurately reflect changes within the cerebrospinal fluid or brain when ventilation is altered. Submitted on May 1, 1961

scholarly journals Subdiaphragmatic venous stasis and tissular hypoperfusion as sources of metabolic acidosis during passive portal-jugular and caval-jugular bypasses in dogs

2000 ◽  
Vol 15 (2) ◽  
pp. 94-101 ◽  
Author(s):  
Antônio Roberto de Barros Coelho ◽  
Álvaro Antônio Bandeira Ferraz ◽  
Renato Dornelas Câmara Neto ◽  
Ayrton Ponce de Souza ◽  
Edmundo Machado Ferraz
Keyword(s):  
Carbon Dioxide ◽  
Liver Transplantation ◽  
Metabolic Acidosis ◽  
Venous Blood ◽  
Blood Stasis ◽  
Carbon Dioxide Tension ◽  
Base Deficit ◽  
Venous Stasis ◽  
Acid Base ◽  
Arterial Blood

Subdiafragmatic venous decompression during anhepatic stage of canine orthotopic liver transplantation attenuates portal and caval blood stasis and minimize hipoperfusion and metabolic acidosis observed with occlusion of portal and caval veins. During two hours, six dogs submitted to portal-jugular and caval-jugular passive shunts, with maintenance of arterial hepatic flow, were evaluated for pH, carbon dioxide tension (PCO2), base deficit (BD) and oxygen tension (PO2) in portal, caval and systemic arterial blood, as well as for increments of BD (DBD) in portal and caval blood. With a confidence level of 95%, the results showed that: 1. There were not changes of pH anDBD in portal and systemic arterial blood in the majority of studied times; 2. There was metabolic acidosis in caval blood; 3. The negative increments of BD (DBD) were higher in caval blood than in splancnic venous blood at T10, T30 and T105; and, 4. Deoxigenation of portal and caval blood were detected. Acid-base metabolism and oxigenation monitoring of subdiaphramatic venous blood can constitute an effective way to evaluate experimental passive portal-jugular and caval-jugular bypass in dogs.

Clinical evaluation of an instrument to measure carbon dioxide tension at the oxygenator gas outlet in cardiopulmonary bypass

Perfusion ◽  
2006 ◽  
Vol 21 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Frode Kristiansen ◽  
Jan Olav Høgetveit ◽  
Thore H Pedersen
Keyword(s):  
Carbon Dioxide ◽  
Cardiopulmonary Bypass ◽  
Venous Blood ◽  
Carbon Dioxide Tension ◽  
Circuit Board ◽  
Separate Analysis ◽  
Blood Gas ◽  
Arterial Blood ◽  
Gas Measurement ◽  
Venous Blood Gas

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.

Cerebral acid-base and gas metabolism in brain injury

1970 ◽  
Vol 33 (5) ◽  
pp. 498-505 ◽  
Author(s):  
R. Zupping
Keyword(s):  
Metabolic Acidosis ◽  
Brain Injury ◽  
Brain Damage ◽  
Close Correlation ◽  
Respiratory Alkalosis ◽  
Acid Base ◽  
Content Type ◽  
Arterial Blood ◽  
Gas Metabolism ◽  
Permanent Brain Damage

✓ Acid-base and gas parameters of CSF, jugular venous and arterial blood were measured in 45 patients with brain injury in the first 12 days after trauma or operation. CSF metabolic acidosis together with respiratory alkalosis and hypoxemia in the cerebral venous and arterial blood were the most characteristic findings. A close correlation between the severity of brain damage and the intensity of the CSF metabolic acidosis and arterial hypocapnia was revealed. It was concluded that brain hypoxia and acidosis play an important role in the development of cerebral edema and permanent brain damage.

Changes in brain surface pH during acute isocapnic metabolic acidosis and alkalosis

1981 ◽  
Vol 51 (2) ◽  
pp. 276-281 ◽  
Author(s):  
S. Javaheri ◽  
A. Clendening ◽  
N. Papadakis ◽  
J. S. Brody
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Interstitial Fluid ◽  
Acid Base ◽  
Surface Ph ◽  
Brain Surface ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
The Mean ◽  
The Brain

It has been thought that the blood-brain barrier is relatively impermeable to changes in arterial blood H+ and OH- concentrations. We have measured the brain surface pH during 30 min of isocapnic metabolic acidosis or alkalosis induced by intravenous infusion of 0.2 N HCl or NaOH in anesthetized dogs. The mean brain surface pH fell significantly by 0.06 and rose by 0.04 pH units during HCl or NaOH infusion, respectively. Respective changes were also observed in the calculated cerebral interstitial fluid [HCO-3]. There were no significant changes in cisternal cerebrospinal fluid acid-base variables. It is concluded that changes in arterial blood H+ and OH- concentrations are reflected in brain surface pH relatively quickly. Such changes may contribute to acute respiratory adaptations in metabolic acidosis and alkalosis.

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