BJA
Correspondence
removal and induces a strong upstroke in E′CO2 when ventilation is restarted. So, the relatively small changes in cardiac output that could occur in the same time will not be detected. Finally, this raises a major methodological question. As the methods are described, it seems that the authors measured ′ ECO not after restarting ventilation, but at the end of EEO. It is 2 hard to understand how it is possible to measure E′CO2 on the exhaled gas . . . during an occlusion of the respiratory circuit. Overall, contradicting previous publications should require to use accurate methods and to construct one’s reasoning on the most obvious physiological basis.
Declaration of interest X.M. and J.-L.T. are members of the Medical Advisory Board of Pulsion Medical Systems.
1 Guinot PG, Godart J, de Broca B, Bernard E, Lorne E, Dupont H. End-expiratory occlusion manoeuvre does not accurately predict fluid responsiveness in the operating theatre. Br J Anaesth 2014; 112: 1050– 4 2 Monnet X, Chemla D, Osman D, et al. Measuring aortic diameter improves accuracy of esophageal Doppler in assessing fluid responsiveness. Crit Care Med 2007; 35: 477–82
doi:10.1093/bja/aeu430
Clinical practice Reply from the authors Editor—We would like to thank Prof. Monnet for his critical comments that raised two questions regarding our methodological construction. We wished to evaluate end-expiratory occlusion (EEO) in a certain population undergoing surgery. For this purpose, we evaluated stroke volume (SV) and cardiac output (CO) with a device that has been used and validated in this setting. Additionally, we wished to evaluate variations of E′CO2 because E′CO2 is used every day and could be an interesting tool. First, we used oesophageal Doppler (CardioQ) to assess CO, SV, and their changes during EEO manoeuvre and fluid expansion. We agree that CardioQ does not measure aortic diameter and its ability to measure CO can be questioned; we have already discussed this limitation in our paper.1 Despite these concerns, several studies have demonstrated that CardioQ provides good ability to track changes in SV,2 – 4 and can be used to improve outcomes in the operating theatre.5 6 Each cardiac output devices has its limits. Given that aortic diameter varies with aortic pressure, Prof. Monnet demonstrated that aortic blood flow measurement could be influenced by this variable.7 We would like to note that oesophageal Doppler used by Monnet and colleagues may not be equivalent to these used in our study.8 Prof. Monnet used Hemosonic 100 (Arrow
Declaration of interest None declared.
167
Downloaded from http://bja.oxfordjournals.org/ at Johns Hopkins University on June 9, 2015
X. Monnet* J.-L. Teboul Paris, France *E-mail: [email protected]
International, Reading, PA, USA) that may have some inaccuracy of aortic diameter evaluation, which may in turn affect the accuracy of measurement of SV.9 In addition, they did not compare the variations of aortic blood flow measured by Hemosonic to those obtained with a gold standard device, such as thermodilution. Evaluation of CO by CardioQ is based on a nomogram created by calibration of left ventricular SV as measured by the pulmonary artery catheter against descending aortic blood flow velocity and stroke distance as measured by CardioQ. Thus, its nomogram provides a calibration factor to translate the descending aortic blood flow velocity to total CO over a wide range of patient conditions.10 Some clinical situations (such as acute circulatory failure, sepsis, epidural analgesia) may change the relation between aortic diameter and aortic pressure, and percentage split of flow between the upper body and lower body.11 In contrast to the intensive care unit population, none of our patients experienced these events. Regardless of the limitations discussed above, trend monitoring of SV should theoretically be possible as long as conditions of validation remain unaltered. In our study, these conditions remained constant; moreover, none of our patients suffered from severe arterial hypotension and/or were treated with vasoactive drugs during the study period. For these reasons, we believe that CardioQ was able to measure and track changes in SV during the different steps. To note, an abstract evaluating EEO manoeuvre with ODM had similar results.12 The second point raised by Prof. Monnet was the reliability of the EEO-induced changes in E′CO2 . The rate of increase in arterial dioxide carbon in anaesthetized patients is biphasic with a first linear phase above 3–5 mm Hg min21.13 Based on this fact, we hypothesized that an apnoea of 15 s could be assimilated to a short time period not sufficient to create a strong increase in ′ ′ ECO , and that the main changes in ECO could be due to 2 2 changes in SV. As we observed an increase in E′CO2 with no significant correlation between changes of SV and E′CO2 (r¼0.27, P¼0.088), apnoea may have in part increased E′CO2 . Nevertheless, E′CO2 did not track changes of SV for the reason that haemodynamic status in our population was not that of patients with acute circulatory failure. From a physiological point of view, we wonder if our population did not increase oxygen consumption (VO2) with the increase in oxygen delivery (DO2), whereas the population in the intensive care unit or haemodynamically unstable patients do increase VO2 and E′CO2 with an increase in DO2.14 15 There are relatively old studies that have evaluated the relationship between VO2, DO2, and E′CO2 .16 17 These studies demonstrated that when DO2 increases, E′CO2 and VO2 increase together to the critical DO2, then after this point, even large increases in DO2 are not followed by any increase in E′CO2 and VO2.16 17 We believe that was the reason why we did not observe any changes of E′CO2 during fluid expansion, whereas SV did.1
BJA P-G. Guinot* J. Godart B. de Broca E. Bernard E. Lorne H. Dupont Amiens, France *E-mail: [email protected]
168
17 Jin X, Weil MH, Tang W, et al. End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock. Crit Care Med 2000; 28: 2415– 9
doi:10.1093/bja/aeu431
Hazards of bone cement: for patient and operating theatre personnel Editor—We read with great interest the recent article by Schummer and colleagues,1 dealing with the administration of bone cement for vertebroplasty which may lead to pulmonary embolism and potentially devastating consequences if not treated correctly. This may also occur in patients having total knee/hip replacement. We would like to highlight several other less known, albeit dangerous hazards of bone cement. We believe that bone cement is a hazardous mixture when applied to bone fractures and metal prosthesis implants. The cement is dangerous to the patient, but may also be hazardous to the personnel in the room.2 3 These dangers should also be known to anaesthetists. Bone cement, when mixed before application, gives off a very pungent smell and cloud of fumes that operating theatre personnel near the operating table may inhale. This inhalation over time can lead to the nervous system side-effects (causing symptoms similar to drunkenness) with headache, drowsiness, nausea, weakness, fatigue, irritability, dizziness, and loss of appetite. Most people will not experience these nervous system side-effects without first experiencing local irritation to the skin, eyes, nose, or throat. Methyl methacrylate (MMA) vapour at a level of 125 ppm (just above Cal-OSHA’s Permissible Exposure limit) may cause teary eyes, sore throat, coughing, and irritation of the nose. In animal studies, prolonged exposure to 400 ppm damaged the surface of the trachea. It is not known whether this occurs in humans. Moreover, direct skin contact with MMA can cause itching, burning, redness, swelling, and cracking of the skin. Repeated skin contact can cause dermatitis. In some people, an allergic skin reaction can occur. There are reports that prolonged skin contact may cause tingling, numbness, and whitening of the fingers. MMA easily penetrates most ordinary clothing and can also penetrate surgical gloves. Some studies have suggested that MMA can cause birth defects when pregnant animals are exposed to extremely high levels. It is not known whether MMA can affect pregnancy in humans. However, MMA inhaled by a pregnant woman can reach the fetus and women who may be pregnant should avoid overexposure to MMA. Operating theatres should be well ventilated with a laminar flow system to take care of the cement odour and fumes. Rooms can also be constructed with a glass wall partition to separate the operating theatre table and the patient from the operating theatre nurse and other personnel.
Declaration of interest None declared.
Downloaded from http://bja.oxfordjournals.org/ at Johns Hopkins University on June 9, 2015
1 Guinot PG, Godart J, de Broca B, Bernard E, Lorne E, Dupont H. End-expiratory occlusion manoeuvre does not accurately predict fluid responsiveness in the operating theatre. Br J Anaesth 2014; 112: 1050–4 2 Valtier B, Cholley BP, Belot JP, de la Coussaye JE, Mateo J, Payen DM. Noninvasive monitoring of cardiac output in critically ill patients using transesophageal Doppler. Am J Respir Crit Care Med 1998; 158: 77– 83 3 Roeck M, Jakob SM, Boehlen T, Brander L, Knuesel R, Takala J. Change in stroke volume in response to fluid challenge: assessment using esophageal Doppler. Intensive Care Med 2003; 29: 1729– 35 4 Kim K, Kwok I, Chang H, Han T. Comparison of cardiac outputs of major burn patients undergoing extensive early escharectomy: esophageal Doppler monitor versus thermodilution pulmonary artery catheter. J Trauma 2004; 57: 1013– 7 5 Gan TJ, Soppitt A, Maroof M, et al. Goal-directed intraoperative fluid administration reduces length of hospital stay after major surgery. Anesthesiology 2002; 97: 820– 6 6 Dark PM, Singer M. The validity of trans-esophageal Doppler ultrasonography as a measure of cardiac output in critically ill adults. Intensive Care Med 2004; 30: 2060–6 7 Monnet X, Chemla D, Osman D, et al. Measuring aortic diameter improves accuracy of esophageal Doppler in assessing fluid responsiveness. Crit Care Med 2007; 35: 477– 82 8 Schober P, Loer SA, Schwarte LA. Perioperative hemodynamic monitoring with transesophageal Doppler technology. Anesth Analg 2009; 109: 340– 53 9 Cariou A, Monchi M, Joly LM, et al. Noninvasive cardiac output monitoring by aortic blood flow determination: evaluation of the Sometec Dynemo-3000 system. Crit Care Med 1998; 26: 2066– 72 10 Singer M. ODM/CardioQ esophageal Doppler technology. Crit Care Med 2003; 31: 1888– 9 11 Leather HA, Wouters PF. Oesophageal Doppler monitoring overestimates cardiac output during lumbar epidural anaesthesia. Br J Anaesth 2001; 86: 794–7 12 Weil G, Suria S, Monnet X. Prediction de la reponse au remplissage par un test de pause tele-expiratoire pendant une chirurgie abdominale. Ann Fr Anesth Reanim 2013; 32(Suppl. 1): A287 13 Frumin J, Epstein RM, Cohen G. Apneic oxygenation in man. Anesthesiology 1954; 20: 789– 98 14 Young A, Marik PE, Sibole S, Grooms D, Levitov A. Changes in end tidal carbon dioxide and volumetric carbon dioxide as predictors of volume responsiveness in hemodynamically unstable patients. J Cardiothorac Vasc Anesth 2013; 27: 681– 4 15 Monnet X, Bataille A, Magalhaes E, et al. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test. Intensive Care Med 2013; 39: 93 – 100 16 Guzman JA, Lacoma FJ, Najar A, Kruse JA. End-tidal partial pressure of carbon dioxide as a noninvasive indicator of systemic oxygen supply dependency during hemorrhagic shock and resuscitation. Shock 1997; 8: 427–31
Correspondence
Correspondence
removal and induces a strong upstroke in E′CO2 when ventilation is restarted. So, the relatively small changes in cardiac output that could occur in the same time will not be detected. Finally, this raises a major methodological question. As the methods are described, it seems that the authors measured ′ ECO not after restarting ventilation, but at the end of EEO. It is 2 hard to understand how it is possible to measure E′CO2 on the exhaled gas . . . during an occlusion of the respiratory circuit. Overall, contradicting previous publications should require to use accurate methods and to construct one’s reasoning on the most obvious physiological basis.
Declaration of interest X.M. and J.-L.T. are members of the Medical Advisory Board of Pulsion Medical Systems.
1 Guinot PG, Godart J, de Broca B, Bernard E, Lorne E, Dupont H. End-expiratory occlusion manoeuvre does not accurately predict fluid responsiveness in the operating theatre. Br J Anaesth 2014; 112: 1050– 4 2 Monnet X, Chemla D, Osman D, et al. Measuring aortic diameter improves accuracy of esophageal Doppler in assessing fluid responsiveness. Crit Care Med 2007; 35: 477–82
doi:10.1093/bja/aeu430
Clinical practice Reply from the authors Editor—We would like to thank Prof. Monnet for his critical comments that raised two questions regarding our methodological construction. We wished to evaluate end-expiratory occlusion (EEO) in a certain population undergoing surgery. For this purpose, we evaluated stroke volume (SV) and cardiac output (CO) with a device that has been used and validated in this setting. Additionally, we wished to evaluate variations of E′CO2 because E′CO2 is used every day and could be an interesting tool. First, we used oesophageal Doppler (CardioQ) to assess CO, SV, and their changes during EEO manoeuvre and fluid expansion. We agree that CardioQ does not measure aortic diameter and its ability to measure CO can be questioned; we have already discussed this limitation in our paper.1 Despite these concerns, several studies have demonstrated that CardioQ provides good ability to track changes in SV,2 – 4 and can be used to improve outcomes in the operating theatre.5 6 Each cardiac output devices has its limits. Given that aortic diameter varies with aortic pressure, Prof. Monnet demonstrated that aortic blood flow measurement could be influenced by this variable.7 We would like to note that oesophageal Doppler used by Monnet and colleagues may not be equivalent to these used in our study.8 Prof. Monnet used Hemosonic 100 (Arrow
Declaration of interest None declared.
167
Downloaded from http://bja.oxfordjournals.org/ at Johns Hopkins University on June 9, 2015
X. Monnet* J.-L. Teboul Paris, France *E-mail: [email protected]
International, Reading, PA, USA) that may have some inaccuracy of aortic diameter evaluation, which may in turn affect the accuracy of measurement of SV.9 In addition, they did not compare the variations of aortic blood flow measured by Hemosonic to those obtained with a gold standard device, such as thermodilution. Evaluation of CO by CardioQ is based on a nomogram created by calibration of left ventricular SV as measured by the pulmonary artery catheter against descending aortic blood flow velocity and stroke distance as measured by CardioQ. Thus, its nomogram provides a calibration factor to translate the descending aortic blood flow velocity to total CO over a wide range of patient conditions.10 Some clinical situations (such as acute circulatory failure, sepsis, epidural analgesia) may change the relation between aortic diameter and aortic pressure, and percentage split of flow between the upper body and lower body.11 In contrast to the intensive care unit population, none of our patients experienced these events. Regardless of the limitations discussed above, trend monitoring of SV should theoretically be possible as long as conditions of validation remain unaltered. In our study, these conditions remained constant; moreover, none of our patients suffered from severe arterial hypotension and/or were treated with vasoactive drugs during the study period. For these reasons, we believe that CardioQ was able to measure and track changes in SV during the different steps. To note, an abstract evaluating EEO manoeuvre with ODM had similar results.12 The second point raised by Prof. Monnet was the reliability of the EEO-induced changes in E′CO2 . The rate of increase in arterial dioxide carbon in anaesthetized patients is biphasic with a first linear phase above 3–5 mm Hg min21.13 Based on this fact, we hypothesized that an apnoea of 15 s could be assimilated to a short time period not sufficient to create a strong increase in ′ ′ ECO , and that the main changes in ECO could be due to 2 2 changes in SV. As we observed an increase in E′CO2 with no significant correlation between changes of SV and E′CO2 (r¼0.27, P¼0.088), apnoea may have in part increased E′CO2 . Nevertheless, E′CO2 did not track changes of SV for the reason that haemodynamic status in our population was not that of patients with acute circulatory failure. From a physiological point of view, we wonder if our population did not increase oxygen consumption (VO2) with the increase in oxygen delivery (DO2), whereas the population in the intensive care unit or haemodynamically unstable patients do increase VO2 and E′CO2 with an increase in DO2.14 15 There are relatively old studies that have evaluated the relationship between VO2, DO2, and E′CO2 .16 17 These studies demonstrated that when DO2 increases, E′CO2 and VO2 increase together to the critical DO2, then after this point, even large increases in DO2 are not followed by any increase in E′CO2 and VO2.16 17 We believe that was the reason why we did not observe any changes of E′CO2 during fluid expansion, whereas SV did.1
BJA P-G. Guinot* J. Godart B. de Broca E. Bernard E. Lorne H. Dupont Amiens, France *E-mail: [email protected]
168
17 Jin X, Weil MH, Tang W, et al. End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock. Crit Care Med 2000; 28: 2415– 9
doi:10.1093/bja/aeu431
Hazards of bone cement: for patient and operating theatre personnel Editor—We read with great interest the recent article by Schummer and colleagues,1 dealing with the administration of bone cement for vertebroplasty which may lead to pulmonary embolism and potentially devastating consequences if not treated correctly. This may also occur in patients having total knee/hip replacement. We would like to highlight several other less known, albeit dangerous hazards of bone cement. We believe that bone cement is a hazardous mixture when applied to bone fractures and metal prosthesis implants. The cement is dangerous to the patient, but may also be hazardous to the personnel in the room.2 3 These dangers should also be known to anaesthetists. Bone cement, when mixed before application, gives off a very pungent smell and cloud of fumes that operating theatre personnel near the operating table may inhale. This inhalation over time can lead to the nervous system side-effects (causing symptoms similar to drunkenness) with headache, drowsiness, nausea, weakness, fatigue, irritability, dizziness, and loss of appetite. Most people will not experience these nervous system side-effects without first experiencing local irritation to the skin, eyes, nose, or throat. Methyl methacrylate (MMA) vapour at a level of 125 ppm (just above Cal-OSHA’s Permissible Exposure limit) may cause teary eyes, sore throat, coughing, and irritation of the nose. In animal studies, prolonged exposure to 400 ppm damaged the surface of the trachea. It is not known whether this occurs in humans. Moreover, direct skin contact with MMA can cause itching, burning, redness, swelling, and cracking of the skin. Repeated skin contact can cause dermatitis. In some people, an allergic skin reaction can occur. There are reports that prolonged skin contact may cause tingling, numbness, and whitening of the fingers. MMA easily penetrates most ordinary clothing and can also penetrate surgical gloves. Some studies have suggested that MMA can cause birth defects when pregnant animals are exposed to extremely high levels. It is not known whether MMA can affect pregnancy in humans. However, MMA inhaled by a pregnant woman can reach the fetus and women who may be pregnant should avoid overexposure to MMA. Operating theatres should be well ventilated with a laminar flow system to take care of the cement odour and fumes. Rooms can also be constructed with a glass wall partition to separate the operating theatre table and the patient from the operating theatre nurse and other personnel.
Declaration of interest None declared.
Downloaded from http://bja.oxfordjournals.org/ at Johns Hopkins University on June 9, 2015
1 Guinot PG, Godart J, de Broca B, Bernard E, Lorne E, Dupont H. End-expiratory occlusion manoeuvre does not accurately predict fluid responsiveness in the operating theatre. Br J Anaesth 2014; 112: 1050–4 2 Valtier B, Cholley BP, Belot JP, de la Coussaye JE, Mateo J, Payen DM. Noninvasive monitoring of cardiac output in critically ill patients using transesophageal Doppler. Am J Respir Crit Care Med 1998; 158: 77– 83 3 Roeck M, Jakob SM, Boehlen T, Brander L, Knuesel R, Takala J. Change in stroke volume in response to fluid challenge: assessment using esophageal Doppler. Intensive Care Med 2003; 29: 1729– 35 4 Kim K, Kwok I, Chang H, Han T. Comparison of cardiac outputs of major burn patients undergoing extensive early escharectomy: esophageal Doppler monitor versus thermodilution pulmonary artery catheter. J Trauma 2004; 57: 1013– 7 5 Gan TJ, Soppitt A, Maroof M, et al. Goal-directed intraoperative fluid administration reduces length of hospital stay after major surgery. Anesthesiology 2002; 97: 820– 6 6 Dark PM, Singer M. The validity of trans-esophageal Doppler ultrasonography as a measure of cardiac output in critically ill adults. Intensive Care Med 2004; 30: 2060–6 7 Monnet X, Chemla D, Osman D, et al. Measuring aortic diameter improves accuracy of esophageal Doppler in assessing fluid responsiveness. Crit Care Med 2007; 35: 477– 82 8 Schober P, Loer SA, Schwarte LA. Perioperative hemodynamic monitoring with transesophageal Doppler technology. Anesth Analg 2009; 109: 340– 53 9 Cariou A, Monchi M, Joly LM, et al. Noninvasive cardiac output monitoring by aortic blood flow determination: evaluation of the Sometec Dynemo-3000 system. Crit Care Med 1998; 26: 2066– 72 10 Singer M. ODM/CardioQ esophageal Doppler technology. Crit Care Med 2003; 31: 1888– 9 11 Leather HA, Wouters PF. Oesophageal Doppler monitoring overestimates cardiac output during lumbar epidural anaesthesia. Br J Anaesth 2001; 86: 794–7 12 Weil G, Suria S, Monnet X. Prediction de la reponse au remplissage par un test de pause tele-expiratoire pendant une chirurgie abdominale. Ann Fr Anesth Reanim 2013; 32(Suppl. 1): A287 13 Frumin J, Epstein RM, Cohen G. Apneic oxygenation in man. Anesthesiology 1954; 20: 789– 98 14 Young A, Marik PE, Sibole S, Grooms D, Levitov A. Changes in end tidal carbon dioxide and volumetric carbon dioxide as predictors of volume responsiveness in hemodynamically unstable patients. J Cardiothorac Vasc Anesth 2013; 27: 681– 4 15 Monnet X, Bataille A, Magalhaes E, et al. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test. Intensive Care Med 2013; 39: 93 – 100 16 Guzman JA, Lacoma FJ, Najar A, Kruse JA. End-tidal partial pressure of carbon dioxide as a noninvasive indicator of systemic oxygen supply dependency during hemorrhagic shock and resuscitation. Shock 1997; 8: 427–31
Correspondence
