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LETTER TO EDITOR Table of Contents   
Year : 2010  |  Volume : 13  |  Issue : 3  |  Page : 269-271
Correlation between central venous-arterial carbon dioxide tension gradient and cardiac index changes following fluid therapy


Department of Anesthesia and Surgical Intensive Care, Hotel-Dieu de France Hospital, Saint-Joseph University, Beirut, Lebanon

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Date of Web Publication6-Sep-2010
 

How to cite this article:
Yazigi A, Abou-Zeid H, Haddad F, Madi-Jebara S, Hayeck G, Jabbour K. Correlation between central venous-arterial carbon dioxide tension gradient and cardiac index changes following fluid therapy. Ann Card Anaesth 2010;13:269-71

How to cite this URL:
Yazigi A, Abou-Zeid H, Haddad F, Madi-Jebara S, Hayeck G, Jabbour K. Correlation between central venous-arterial carbon dioxide tension gradient and cardiac index changes following fluid therapy. Ann Card Anaesth [serial online] 2010 [cited 2019 Oct 17];13:269-71. Available from: http://www.annals.in/text.asp?2010/13/3/269/69079


The Editor,

Measurement of mixed venous-arterial carbon dioxide (MVA-CO 2 ) tension gradient is useful in assessing tissue perfusion in critically ill patients. [1],[2] However, mixed venous CO 2 tension measurement is obtained only from a correctly positioned pulmonary artery catheter. The insertion of these catheters is associated with significant risks, increased health care costs and its risk/benefit ratio is a matter of debate. [3] Central venous CO 2 tension, obtained in a less risky and costly manner from a central venous catheter, may be an interesting alternative to mixed venous CO 2 tension measurement. Central venous-arterial carbon dioxide (CVA-CO 2 ) tension gradient was shown to have a negative and significant correlation with cardiac index (CI) of patients in sepsis [4] and in circulatory failure. [5] The aim of this study was to correlate the changes of CVA-CO 2 tension gradient and CI in patients receiving fluid therapy following coronary surgery. A significant correlation between the changes of CVA-CO 2 tension gradient and CI would make CVA-CO 2 gradient a valuable indicator to assess the effect of volume loading on CI following coronary surgery.

Forty adult patients, with a CI <2.5 l/min/m΂ at the time of admission in the intensive care unit following elective coronary surgery, were consecutively included in this prospective study. Institutional review board was obtained and informed written consent was given by all patients. Exclusion criteria were a pulmonary artery occlusion pressure above 12 mm Hg, intracardiac shunting, active bleeding, inotropic drugs or hemodynamic mechanical assistance. Invasive monitoring was achieved with a 20-gauge radial artery catheter (Plastimed, Saint-Lieu-la-Forκt, France) and a 7.5 French pulmonary artery catheter (Edwards Lifesciences, Irvine, CA, USA) with a proximal port positioned in the superior venacava. Arterial, pulmonary artery and central venous pressures were displayed on an electronic monitor (Hellige SMU 611, Freiburg, Germany) and measured at end-expiration. Cardiac output was obtained by the thermodilution technique. CI was computed by averaging three consecutive measurements of cardiac output divided by the patient body surface area.

Patients included in the study had a 500-ml bolus of an isotonic crystalloid solution administered over 20 min. Fluid therapy was stopped if pulmonary artery occlusion pressure reached 18 mm Hg. Concomitant hemodynamic and blood gases measurements were taken in included patients immediately before starting fluid therapy (T0) and were repeated at the end of the loading manoeuvre (T1). Blood samples of 2 ml were simultaneously obtained from the radial artery catheter and from the proximal port of the pulmonary artery catheter after withdrawal of dead space blood and flushing fluid. All samples were withdrawn over 30 seconds, using a low-negative pressure technique. Samples were immediately analyzed for blood gas variables using a blood gas analyzer (ABL, Radiometer, Copenhagen, Denmark) calibrated according to the standards supplied by the manufacturer. During the study period, patients were sedated and mechanically ventilated with a tidal volume of 10 ml/kg, an FIO 2 of 60% and a respiratory rate of 12/min. Body temperature was maintained with a warming blanket.

On the basis of a preliminary investigation that showed a correlation coefficient of 0.4 between CVA-CO 2 gradient and CI changes following fluid therapy, it was determined that a sample of 36 patients is needed to demonstrate a significant correlation, with a power of 80% and an a coefficient of 0.05, between the two primary evaluated parameters in our study. Data were presented as mean ± standard deviation and were compared by paired Student's t-test. Changes in individual values of CVA-CO 2 tension gradient and CI were recorded as CVA-CO 2 gradient and DCI. The correlation between DCVA-CO 2 gradient and CI was evaluated by linear regression analysis and Spearman test. P ͳ 0.05 was considered to be statistically significant.

All the patients responded to volume loading without increasing pulmonary artery occlusion pressure above 18 mm Hg. CI was higher at T1 compared to T0 (1.9±0.2 vs. 2.3±0.4 l/min/m΂; P = 0.001). There was a significant decrease of CVA-CO 2 tension gradient at T1 compared to T0 (12.2±3.6 vs. 10.1±3.8 mm Hg; P = 0.01). The correlation between DCVA-CO 2 gradient and DCI, shown in [Figure 1], was negative and statistically significant (r = -0.53; P = 0.001).
Figure 1: The correlation between CVA-CO2 tension gradient changes and CI changes from T0 to T1

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The results of this study have clinical implications. In a resource-limited context where pulmonary artery catheters or other monitoring techniques might not be available, measurement of DCVA-CO 2 gradient can be used to assess the impact of volume loading on CI. An inadequate decrease in CVA-CO 2 tension gradient after volume expansion may indicate the need for additional or alternative resuscitative measures. Recently, Vallιe et al, showed that in resuscitated septic shock patients, the persistence of a CVA-CO 2 tension gradient above 6 mm Hg indicated the need of further therapies. [ 6] Following this pilot study, more investigations are needed to assess the correlation between CVA-CO 2 and CI changes following fluid loading in patients with poor ventricular function or valve diseases. Further studies are also required to evaluate how CVA-CO 2 gradient changes could be used to assess the impact of various hemodynamic therapeutic modalities.as vasoactive or inotropic drugs.

 
   References Top

1.Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL, Griffel MI. Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med 1986;315:153-6.   Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Mekontso-Dessap A, Castelain V, Anguel N, Bahloul M, Schauvliege F, Richard C, et al. Combination of venoarterial PCO2 difference with arteriovenous O 2 content difference to detect anaerobic metabolism in patients. Intensive Care Med 2002;28:272-7.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Djaiani G, Karski J, Yudin M, Hynninen M, Fedorko L, Carroll J, et al. Clinical outcomes in patients undergoing elective coronary artery bypass graft surgery with and without utilization of pulmonary artery catheter-generated data. J Cardiothorac Vasc Anesth 2006;20:307-10.   Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Cuschieri J, Rivers EP, Donnino MW, Katilius M, Jacobsen G, Nguyen HB, Pamukov N, et al. Central venous-arterial carbon dioxide difference as an indicator of cardiac index. Intensive Care Med 2005;31:818-22.   Back to cited text no. 4  [PUBMED]  [FULLTEXT]  
5.Ho KM, Harding R, Chamberlain J. A comparison of central venous-arterial and mixed venous-arterial carbon dioxide tension gradient in circulatory failure. Anaesth Intensive Care 2007;35:695-701.   Back to cited text no. 5  [PUBMED]    
6.Vallιe F, Vallet B, Mathe O, Parraguette J, Mari A, Silva S, et al. Central venous-to-arterial carbon dioxide difference: an additional target for goal-directed therapy in septic shock? Intensive Care Med 2008;34:2218-25.  Back to cited text no. 6      

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Correspondence Address:
Alexandre Yazigi
Department of Anesthesia and Surgical Intensive Care, Hotel-Dieu de France Hospital, Saint-Joseph University, Beirut
Lebanon
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.69079

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