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Ann Thorac Surg 2000;70:1098-1099
© 2000 The Society of Thoracic Surgeons
a Maimonides Medical Center and State University of New York, Downstate Medical Center, Brooklyn, New York, USA
Address reprint requests to Dr Reddy, Department of Cardiovascular and Thoracic Surgery, State University of New York, Downstate Medical Center, 450 Clarkson Ave, Box 40, Brooklyn, NY 11203-2098
e-mail: ramreddy{at}aol.com
Presented at the Sixth Annual Cardiothoracic Techniques and Technologies Meeting 2000, Ft Lauderdale, FL, Jan 2729, 2000.
| Abstract |
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Methods. Five hemodynamic and respiratory parameters (end-tidal carbon dioxide, arterial partial pressure of carbon dioxide, mean arterial pressure, mean pulmonary arterial pressure, and cardiac output), were measured in 100 consecutive patients undergoing EVH with CO2 insufflation. Data were obtained prior to commencement of EVH, 15 minutes after commencement, and 5 minutes after completion of the vein harvesting.
Results. No adverse hemodynamic effects were observed during CO2 insufflation. Specifically, average mean arterial pressure went from 88.77 ± 9.64 to 89.13 ± 8.60 to 88.24 ± 8.71 mm Hg before, during, and after endoscopic vein harvesting (p = 0.291). Likewise, average mean pulmonary artery pressures were 19.76 ± 4.75, 20.05 ± 4.48, and 20.05 ± 4.62 mm Hg (p = 0.547); and average cardiac output was 4.25 ± 0.74, 4.22 ± 0.73, and 4.23 ± 0.69 L/min (p = 0.109) at those three intervals. Additionally, there was no evidence of significant systemic absorption of CO2 as reflected in average arterial PCO2, which remained steady at 37.42 ± 5.19, 37.51 ± 4.59, and 38.10 ± 4.80 mm Hg (p = 0.217); and average end-tidal CO2, which was 32.10 ± 3.66, 32.50 ± 3.47, and 32.38 ± 3.33 mm Hg (p = 0.335). In a subset of 20 patients with elevated pulmonary arterial pressure (more than 32 mm Hg), there was also no significant change in any of the parameters.
Conclusions. Carbon dioxide insufflation during EVH leads to no adverse hemodynamic consequences or systemic CO2 absorption. The technique appears to be safe and well tolerated.
| Introduction |
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Patients undergoing CO2 pneumoperitonium with concomitant cardiopulmonary disease have been shown to retain CO2 gas and develop arterial hypercapnia and subsequent arterial acidosis [2]. This retention has also been documented to a lesser extent in otherwise healthy individuals [3]. CO2-related cardiopulmonary dysfunction and hypercapnia have also been shown to occur with extraperitoneal and subcutaneous insufflation [4, 5].
This prospective clinical study was performed to determine the possible adverse hemodynamic effects of subcutaneous CO2 insufflation in our increasingly elderly and sick patients undergoing coronary artery bypass grafting (CABG).
| Material and methods |
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Concomitantly to the sternotomy, a 2-cm incision was made in the lower thigh to perform the EVH. After the saphenous vein was identified, a 12-mm blunt-tipped trocar was inserted into the incision to create a seal for CO2 insufflation through a side port in the trocar. A low flow of CO2 (4 L/min), was begun to maintain a cavity pressure of 12 mm Hg. The insufflator (Karl Storz-electronic endoflator #2643050, Tuttingen, Germany), was capable of regulating the gas flow and maintaining a constant positive pressure in the closed space.
Values for each of the five hemodynamic variables were obtained at base line, 15 minutes into the EVH procedure, and 5 minutes after completion of EVH. Statistical analysis was performed using repeated-measures analysis of variance. All values are expressed as the mean ± standard deviation.
| Results |
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The institution of CO2 insufflation did not produce a significant alteration in MAP. The MAP was 88.77 ± 9.64 mm Hg at base line. After the initiation of CO2 insufflation, the MAP was 89.13 ± 8.60 mm Hg, and at the conclusion of EVH it was 88.24 ± 8.71 mm Hg (p = 0.291).
The ETCO2 was not significantly altered by the insufflation of CO2. The mean base line ETCO2 was 32.10 ± 3.66 mm Hg. It was 32.50 ± 3.47 mm Hg after the initiation of CO2 insufflation and 32.38 ± 3.33 mm Hg at the conclusion of EVH (p = 0.335).
The PCO2 at base line was 37.42 ± 5.19 mm Hg. It was 37.51 ± 4.59 mm Hg after beginning CO2 insufflation and at the conclusion of EVH; it was 38.10 ± 4.80 mm Hg (p = 0.217).
There was no significant change in MPAP during CO2 insufflation. At base line the MPAP was 19.76 ± 4.75 mm Hg. It was 20.05 ± 4.48 mm Hg during CO2 insufflation and 20.05 ± 4.62 mm Hg at the conclusion of EVH (p = 0.547).
Cardiac output remained stable throughout the EVH procedure. The cardiac output at base line was 4.15 ± 0.74 L/min. During CO2 insufflation it was 4.22 ± 0.73 L/min and 4.23 ± 0.69 L/min at the conclusion of EVH (p = 1.09).
In the subset of 23 patients with elevated PAP (higher than 35 mm Hg) similar analysis of all of the parameters again failed to reveal any significant changes attributable to CO2 insufflation. The PA systolic pressures at the three time periods were 39.25 ± 4.30, 38.4 ± 4.02 and 39 ± 4.93 mm Hg, respectively (p = 0.255). The PA diastolic pressures were 20.95 ± 3.43, 20.5 ± 3.56, and 19.95 ± 4.80 mm Hg with a p value of 0.183. Also, the PaCO2 values were 38.33 ± 6.38, 39.14 ± 6.20, and 39.62 ± 6.14 mm Hg, respectively (p = 0.10).
| Comment |
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Our results are relatively consistent with the literature. Rudston-Brown and colleagues [5] showed in a porcine model that subcutaneous insufflation of CO2 was indeed associated with hypercapnia and respiratory acidosis. They, however, found that the extent of the subcutaneous emphysema and certainly the extent of the hypercarbia and acidosis were related to the total volume of CO2 insufflated [5]. Clearly the use of low flow CO2 insufflation at 4 L/min and a pressure of 12 mm Hg may be an important reason why there was minimal change seen in our patients. Also given the fact that instrument changes intermittently caused the collapse of the cavity and therefore the removal of CO2 from the subcutaneous space probably helped to keep the effects to a minimal level. It is conceivable that if higher flows and higher pressures are used, the CO2 gradient across the tissue would be sufficient to cause a rise in the CO2 and possibly hemodynamic alterations. It would therefore be our recommendation that careful attention be paid to the flow rate and the pressure of CO2 insufflation while performing EVH.
Hypercapnia has been shown to occur following CO2 pneumoperitoneum, as well as following extraperitoneal procedures and other subcutaneous insufflations as well [2, 46]. Furthermore, the hypercapnia associated with laparoscopy has been shown to be increased in patients who have severe subcutaneous emphysema, suggesting that subcutaneous absorption of CO2 must occur and is an important component of the production of hypercapnia [5]. Because hypercarbia stimulates the sympathetic nervous system and affects the blood pressure and heart rate and causes a risk of dysrhythmia, it clearly should be avoided in elderly debilitated patients undergoing cardiopulmonary procedures [2]. Rudston-Brown and coworkers [5] demonstrated a 30% increase in CO2 load simply from absorption in young healthy adults. It is clear that in patients with advanced emphysema, the results would be particularly troubling and there have indeed been reports of CO2 retention in these patients. Of our 100 patients there were 20 with elevated PAP (higher than 35 mm Hg) under anesthesia. It is instructive to see that even in these patients there was no major rise in CO2 or alterations in hemodynamic parameters.
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