Hypercapnia Improves Tissue Oxygenation

2002 ◽  
Vol 97 (4) ◽  
pp. 801-806 ◽  
Author(s):  
Ozan Akça ◽  
Anthony G. Doufas ◽  
Nobutada Morioka ◽  
Steve Iscoe ◽  
Joseph Fisher ◽  
...  

Background Wound infections are common, serious, surgical complications. Oxidative killing by neutrophils is the primary defense against surgical pathogens and increasing intraoperative tissue oxygen tension markedly reduces the risk of such infections. Since hypercapnia improves cardiac output and peripheral tissue perfusion, we tested the hypothesis that peripheral tissue oxygenation increases as a function of arterial carbon dioxide tension (PaCO(2)) in anesthetized humans. Methods General anesthesia was induced with propofol and maintained with sevoflurane in 30% oxygen in 10 healthy volunteers. Subcutaneous tissue oxygen tension (PsqO(2)) was recorded from a subcutaneous tonometer. An oximeter probe on the upper arm measured muscle oxygen saturation. Cardiac output was monitored noninvasively. PaCO(2) was adjusted to 20, 30, 40, 50, or 60 mmHg in random order with each concentration being maintained for 45 min.(2) (2) Results Increasing PaCO(2) linearly increased cardiac index and PsqO(2) : PsqO(2) = 35.42 + 0.77 (PaCO(2)), < 0.001. Conclusions The observed difference in PsqO(2) is clinically important because previous work suggests that comparable increases in tissue oxygenation reduced the risk of surgical infection from -8% to 2 to 3%. We conclude that mild intraoperative hypercapnia increased peripheral tissue oxygenation in healthy human subjects, which may improve resistance to surgical wound infections.

2004 ◽  
Vol 100 (2) ◽  
pp. 274-280 ◽  
Author(s):  
Barbara Kabon ◽  
Angelika Nagele ◽  
Dayakar Reddy ◽  
Chris Eagon ◽  
James W. Fleshman ◽  
...  

Background Obesity is an important risk factor for surgical site infections. The incidence of surgical wound infections is directly related to tissue perfusion and oxygenation. Fat tissue mass expands without a concomitant increase in blood flow per cell, which might result in a relative hypoperfusion with decreased tissue oxygenation. Consequently, the authors tested the hypotheses that perioperative tissue oxygen tension is reduced in obese surgical patients. Furthermore, they compared the effect of supplemental oxygen administration on tissue oxygenation in obese and nonobese patients. Methods Forty-six patients undergoing major abdominal surgery were assigned to one of two groups according to their body mass index: body mass index less than 30 kg/m2 (nonobese) or 30 kg/m2 or greater (obese). Intraoperative oxygen administration was adjusted to arterial oxygen tensions of approximately 150 mmHg and approximately 300 mmHg in random order. Anesthesia technique and perioperative fluid management were standardized. Subcutaneous tissue oxygen tension was measured with a polarographic electrode positioned within a subcutaneous tonometer in the lateral upper arm during surgery, in the recovery room, and on the first postoperative day. Postoperative tissue oxygen was also measured adjacent to the wound. Data were compared with unpaired two-tailed t tests and Wilcoxon rank sum test; P < 0.05 was considered statistically significant. Results Intraoperative subcutaneous tissue oxygen tension was significantly less in the obese patients at baseline (36 vs. 57 mmHg; P = 0.002) and with supplemental oxygen administration (47 vs. 76 mmHg; P = 0.014). Immediate postoperative tissue oxygen tension was also significantly less in subcutaneous tissue of the upper arm (43 vs. 54 mmHg; P = 0.011) as well as near the incision (42 vs. 62 mmHg; P = 0.012) in obese patients. In contrast, tissue oxygen tension was comparable in each group on the first postoperative morning. Conclusion Wound and tissue hypoxia were common in obese patients in the perioperative period and most pronounced during surgery. Even with supplemental oxygen tissue, oxygen tension in obese patients was reduced to levels that are associated with a substantial increase in infection risk.


2018 ◽  
Vol 63 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Dorothy A. Perry ◽  
Lindsay M. Thomson ◽  
Frank A. Pigula ◽  
Brian D. Polizzotti ◽  
James A. DiNardo ◽  
...  

1994 ◽  
Vol 22 (1) ◽  
pp. A61 ◽  
Author(s):  
Harriet Williams Hopf ◽  
L Glass-Heidenreich ◽  
J Silva ◽  
F Pearce ◽  
M G Ochsner ◽  
...  

1999 ◽  
Vol 27 (Supplement) ◽  
pp. 176A
Author(s):  
H Hopf ◽  
M Knudson ◽  
N Szaflarski ◽  
D Morabito ◽  
J West ◽  
...  

Anaesthesia ◽  
2007 ◽  
Vol 62 (11) ◽  
pp. 1101-1109 ◽  
Author(s):  
B. Kabon ◽  
A. Kugener ◽  
T. Gruenberger ◽  
M. Niedermayr ◽  
E. Fleischmann ◽  
...  

1995 ◽  
Vol 79 (6) ◽  
pp. 1878-1882 ◽  
Author(s):  
D. M. Rosser ◽  
R. P. Stidwill ◽  
D. Jacobson ◽  
M. Singer

The effect of endotoxin on tissue oxygen tension measured at the bladder epithelium was assessed in spontaneously breathing Sprague-Dawley rats anesthetized with halothane. Hyperdynamic (high cardiac output, group A, n = 6) and hypodynamic (low cardiac output, group B, n = 6) circulatory responses were achieved by intravenous administration of Escherichia coli lipopolysaccharide, 10 mg/kg over 30 min or 20 mg/kg over 1 min, respectively. Comparison was made against sham-operated control rats (group C, n = 6). Aortic and renal blood flows increased in group A and fell in group B (P < 0.001). However, in both groups, bladder epithelial oxygen tension rose significantly compared with control (P < 0.01), despite an increasing metabolic acidosis. This is in contradistinction to previous studies of nonseptic insults where bladder epithelial oxygen tension fell in line with an increasing arterial base deficit. If a raised tissue oxygen tension could be demonstrated in other organ beds, this would suggest that decreased utilization of oxygen rather than reduced tissue oxygen availability is responsible for the apparent anaerobic respiration seen in sepsis.


1995 ◽  
Vol 23 (Supplement) ◽  
pp. A167
Author(s):  
David Zabel ◽  
Harriet Hopf ◽  
Kari Kramer ◽  
Thomas Hunt

2006 ◽  
Vol 14 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Noah A. Rosen ◽  
Harriet W. Hopf ◽  
Thomas K. Hunt

2009 ◽  
Vol 111 (5) ◽  
pp. 988-1000 ◽  
Author(s):  
Tenille E. Ragoonanan ◽  
W Scott Beattie ◽  
C David Mazer ◽  
Albert K.Y. Tsui ◽  
Howard Leong-Poi ◽  
...  

Background Perioperative beta-blockade and anemia are independent predictors of increased stroke and mortality by undefined mechanisms. This study investigated the effect of beta-blockade on cerebral tissue oxygen delivery in an experimental model of blood loss and fluid resuscitation (hemodilution). Methods Anesthetized rats were treated with metoprolol (3 mg x kg) or saline before undergoing hemodilution with pentastarch (1:1 blood volume exchange, 30 ml x kg). Outcomes included cardiac output, cerebral blood flow, and brain (PBrO2) and kidney (PKO2) tissue oxygen tension. Hypoxia inducible factor-1alpha (HIF-1alpha) protein levels were assessed by Western blot. Systemic catecholamines, erythropoietin, and angiotensin II levels were measured. Results Hemodilution increased heart rate, stroke volume, cardiac output (60%), and cerebral blood flow (50%), thereby maintaining PBrO2 despite an approximately 50% reduction in blood oxygen content (P &lt; 0.05 for all). By contrast, PKO2 decreased (50%) under the same conditions (P &lt; 0.05). Beta-blockade reduced baseline heart rate (20%) and abolished the compensatory increase in cardiac output after hemodilution (P &lt; 0.05). This attenuated the cerebral blood flow response and reduced PBrO2 (50%), without further decreasing PKO2. Cerebral HIF-1alpha protein levels were increased in beta-blocked hemodiluted rats relative to hemodiluted controls (P &lt; 0.05). Systemic catecholamine and erythropoietin levels increased comparably after hemodilution in both groups, whereas angiotensin II levels increased only after beta-blockade and hemodilution. Conclusions Cerebral tissue oxygen tension is preferentially maintained during hemodilution, relative to the kidney, despite elevated systemic catecholamines. Acute beta-blockade impaired the compensatory cardiac output response to hemodilution, resulting in a reduction in cerebral tissue oxygen tension and increased expression of HIF-1alpha.


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