The relationship between systemic oxygen uptake and del ivery during moderate hypothermic cardiopulmonary bypass: critical values and effects of vasodilation by hydralazine

Perfusion ◽  
1995 ◽  
Vol 10 (5) ◽  
pp. 315-321 ◽  
Author(s):  
F. Cavaliere ◽  
A. Gennari ◽  
L. Martinelli ◽  
R. Zamparelli ◽  
R. Schiavello
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Venous Blood ◽  
Myocardial Revascularization ◽  
Mixed Venous Blood ◽  
Mean Values ◽  
Hypothermic Cardiopulmonary Bypass ◽  
Blood Flow Increase ◽  
Blood Gas Analyses ◽  
The Relationship

The relationship between oxygen delivery (DO2) and uptake (VO2) has been studied during moderately hypothermic cardiopulmonary bypass (CPB) in 15 patients undergoing myocardial revascularization. As soon as nasopharyngeal temperature was lowered to 32°C, blood flow was decreased from 2.4 to 2.0 l/min/m 2. Arterial and mixed venous blood gas analyses were performed five and eight minutes later and DO2 and VO2 were calculated; VO2 stabilized in five minutes after changing blood flow and neither DO2 nor VO2 values changed three minutes later (DO 2: 217 ± 19 versus 215 ± 17 ml/min/m2; VO2: 63 ± 12 versus 66 ± 14 ml/min/m2). Blood flow then was increased to 2.3 l/min/m2 and DO2 and VO2 were determined again, five minutes later; they both increased significantly, to 243 ± 20 and 74 ± 13 ml/min/m 2, respectively. However, a further blood flow increase to 2.6 l/min/m 2 which caused DO2 to increase to 277 ± 24 ml/min/m 2, did not affect VO2 which was unchanged five minutes later (76 ± 13 ml/min/m2); VO2 dependence on DO2 values higher than 243 ± 20 ml/min/m2 was consequently ruled out. Ten patients, having a mean arterial pressure higher than 80 mmHg, were eventually vasodilated with hydralazine, 0.1 mg/kg intravenously, and DO2 and VO2 were determined after five and ten minutes. As blood flow did not change, DO2 was unaffected while a slight increase in VO2 mean values was observed which was not statistically significant (prior to hydralazine: 78 ± 15 ml/min/m2; five minutes later: 82 ± 17 ml/min/m2; 10 minutes later: 76 ± 18 ml/min/m2). In conclusion, during hypothermic CPB at 32°C, VO2 plateau ranges between 48 and 102 mi/min/m 2 (mean ± 2 SD) in 95% of patients, corresponding to 66 and 141 ml/min/m 2 at 37°C; this finding closely matches other literature reports. Consequently, lower VO2 values suggest inadequate oxygen supply to tissues. Critical DO2 at 32°C is lower than 283 ml/min/m2 in 97.5% of patients. Finally, arterial vasoconstriction does not seem to play a significant role in tissue hypoperfusion.

The relationship between mixed venous and regional venous oxygen saturation during cardiopulmonary bypass

Perfusion ◽  
2002 ◽  
Vol 17 (2) ◽  
pp. 133-139 ◽  
Author(s):  
Lena Lindholm ◽  
Vigdis Hansdottir ◽  
Magnus Lundqvist ◽  
Anders Jeppsson
Keyword(s):  
Cardiopulmonary Bypass ◽  
Oxygen Saturation ◽  
Hepatic Vein ◽  
Jugular Vein ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
Mixed Venous Saturation ◽  
Venous Oxygen Saturation ◽  
The Relationship ◽  
Mixed Venous

The relationship between mixed venous and regional venous saturation during cardiopulmonary bypass (CPB), and whether this relationship is influenced by temperature, has been incompletely elucidated. Thirty patients undergoing valve and/or coronary surgery were included in a prospective, controlled and randomized study. The patients were allocated to two groups: a hypothermic group (28°C) and a tepid group (34°C). Blood gases were analysed in blood from the hepatic vein and the jugular vein and from mixed venous blood collected before surgery, during hypothermia, during rewarming, and 30 min after CPB was discontinued. Oxygen saturation in the hepatic vein was lower than in the mixed venous blood at all times of measurement (-24.0 ± 3.0% during hypothermia, -36.5 ± 2.9% during rewarming, and -30.5 ± 3.0% postoperatively, p < 0.001 at all time points). In 23% of the measurements, the hepatic saturation was < 25% in spite of normal (> 60%) mixed venous saturation. There was a statistical correlation between mixed venous and hepatic vein oxygen saturation (r = 0.76, p < 0.0001). Jugular vein oxygen saturation was lower than mixed venous saturation in all three measurements (-21.6 ± 1.9% during hypothermia, p < 0.001; -16.7 ± 1.9% during rewarming, p < 0.001; and -5.6 ± 2.2% postoperatively, p = 0.037). No significant correlation in oxygen saturation could be detected between mixed venous and jugular vein blood ( r = 0.06, p = 0.65). Systemic temperature did not influence the differences in oxygen saturation between mixed venous and regional venous blood at any time point. In conclusion, regional deoxyge-nation occurs during CPB, in spite of normal mixed venous saturation. Mixed venous oxygen saturation correlates with hepatic, but not with jugular, vein saturation. The level of hypothermia does not influence differences in oxygen saturation between mixed venous and regional venous blood.

A nomogram to evaluate the arterial mixed venous oxygen saturation difference during cardiopulmonary bypass

Perfusion ◽  
1998 ◽  
Vol 13 (1) ◽  
pp. 45-51 ◽  
Author(s):  
F Cavaliere
Keyword(s):  
Cardiopulmonary Bypass ◽  
Muscle Relaxation ◽  
Venous Blood ◽  
Myocardial Revascularization ◽  
The Body ◽  
Mixed Venous Blood ◽  
Blood Haemoglobin ◽  
The Difference ◽  
Mixed Venous ◽  
Saturation Difference

A nomogram providing the arterial mixed venous haemoglobin saturation difference (Sa-vO2) corresponding to normal oxygen consumption (VO2) during cardiopulmonary bypass (CPB) was produced. Normal VO2 during CPB (95.8 ± 20.1 ml/min/m2 at 37°C) was obtained from the literature. The nomogram computes the Sa-vO2 from the body surface, pump flow, blood haemoglobin and patient temperature; a table is also presented which supplies the Sa-vO2 ranges corresponding to VO2 mean ±1 and ±2SD. The nomogram was tested on 10 subjects undergoing CPB for myocardial revascularization. Sa-vO2 was determined by arterial and mixed venous blood oximetry 5, 20, and 35 min after the start of CPB. The measured Sa-vO2 was 27.1 ± 7.2% while Sa-vO2 obtained from the nomogram was 24.9 ± 4.0%, the difference was not statistically significant. Eighteen values (60%) were within the range corresponding to VO2 mean ±1SD. One value was lower than the Sa-vO2 value corresponding to VO2 mean - 2SD and was associated with the lowest value of blood haemoglobin. Two values were higher than the Sa-vO2 value corresponding to VO2 mean + 2SD and were associated with inadequate muscle relaxation. By comparing measured Sa-vO2 values with those obtained by the nomogram and the table, anaesthesiologists and perfusionists can easily detect patients presenting abnormally low or high VO2 values.

Massive Pulmonary Infarction during Total Cardiopulmonary Bypass in Unanesthetized Spontaneously Breathing Lambs

1981 ◽  
Vol 4 (2) ◽  
pp. 76-81 ◽  
Author(s):  
T. Kolobow ◽  
R.G. Spragg ◽  
J.E. Pierce
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Pulmonary Ventilation ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
Pulmonary Infarction ◽  
Cardiopulmonary Support ◽  
Mixed Venous

We provided total cardiopulmonary support for 1-18 hours in unanesthetized tethered lambs by peripheral vascular cannulation, using a roller pump and the spiral membrane lung. Respirations were allowed to remain spontaneous and unaided. A Swan-Ganz catheter was placed for retrograde pulmonary artery blood flow sampling. Within a few minutes following induced ventricular fibrillation the PCO2 of sampled blood flowing retrograde through the lungs fell below 10 mm Hg, the PO2 rose to near 150 mm Hg, the pH rose to above 7.8, and the glucose level fell to less than 20 mg %. All of these values later gradually shifted, approaching mixed venous blood values within minutes. After 1-18 hrs of perfusion the animals went into shock and were sacrificed. At autopsy, the lungs of animals breathing room air were beefy and hemorrhagic. In lambs that were «breathing» CO2 enriched air the retrograde pulmonary artery blood pH and PCO2 was usually maintained close to the mixed venous blood values. The observed pulmonary changes were considerably less abnormal, and the microscopic abnormalities were at times nonexistent. We believe the integrity of pulmonary blood flow is vital to the survival of the lungs as a functioning organ. Cessation of total forward pulmonary blood flow (unlike partial cardiopulmonary bypass), combined with spontaneous pulmonary ventilation, rapidly leads to massive, pulmonary infactions, shock, and death.

Impaired carbon dioxide transport during and after cardiopulmonary bypass

Perfusion ◽  
2000 ◽  
Vol 15 (5) ◽  
pp. 433-439 ◽  
Author(s):  
Franco Cavaliere
Keyword(s):  
Cardiopulmonary Bypass ◽  
Whole Blood ◽  
Coronary Revascularization ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
Blood Gas ◽  
Dissociation Curve ◽  
Carbon Dioxide Transport ◽  
Blood Gas Analyses ◽  
Venous Blood Gas

Changes in the CO2 carrying power of blood were evaluated during and after cardiopulmonary bypass (CPB) by calculating the equation of the whole blood CO2 dissociation curve and the ratio between the arterial-venous differences of CO2 content and CO2 tension (Ra-v). Sixteen patients undergoing normothermic CPB for coronary revascularization were studied; arterial and mixed venous blood gas analyses were performed prior to CPB, at the end of first cardioplegia infusion, 25 and 45 min after CPB commencement and 10 min after the termination of CPB. After CPB commencement, the whole blood CO2 dissociation curve became flatter and did not further change during or after CPB. Ra-v decreased from 1.06 ± 0.16 to 0.72 ± 0.12 ml/mmHg after the start of CPB and did not change significantly during CPB; it was still 0.73 ± 0.13 ml/mmHg after CPB. The data indicate that during CPB the amount of CO2 removed from tissues by 1 litre of blood decreases by about 30% and that impairment in CO2 transport persists after the restoration of physiological circulation. Impairment in CO2 transport is mainly caused by haemodilution, but it could be worsened by acidosis.

scholarly journals The beginnings of cardiac catheterization and the resulting impact on pulmonary medicine

2017 ◽  
Vol 313 (4) ◽  
pp. L651-L658 ◽  
Author(s):  
John B. West
Keyword(s):  
Blood Flow ◽  
Cardiac Catheterization ◽  
Nobel Prize ◽  
Venous Blood ◽  
Interventional Cardiology ◽  
Primary Objective ◽  
Mixed Venous Blood ◽  
Pulmonary Medicine ◽  
Fick Principle ◽  
The Right

The early history of cardiac catheterization has many interesting features. First, although it would be natural to assume that the procedure was initiated by cardiologists, two of the three people who shared the Nobel Prize for the discovery were pulmonologists, while the third was a urologist. The primary objective of the pulmonologists André Cournand and Dickinson Richards was to obtain mixed venous blood from the right heart so that they could use the Fick principle to calculate total pulmonary blood flow. Cournand’s initial catheterization studies were prompted by his reading of an account by Werner Forssmann, who catheterized himself 12 years before. His bold experiment was one of the most bizarre in medical history. In the earliest studies that followed, Cournand and colleagues first passed catheters into the right atrium, and then into the right ventricle, and finally, the pulmonary artery. At the time, the investigators did not appreciate the significance of the low vascular pressures, nor that what they had done would revolutionize interventional cardiology. Within a year, William Dock predicted that there would be a very low blood flow at the top of the upright lung, and he proposed that this was the cause of the apical localization of pulmonary tuberculosis. The fact that the pulmonary vascular pressures are very low has many implications in lung disease. Cardiac catheterization changed the face of investigative cardiology, and its instigators were awarded the Nobel Prize in 1956.

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