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Massive Carbon Dioxide Embolism Caused by a Carbon Dioxide Blower During the Repair of a Coronary Vein During Off-Pump Coronary Artery Bypass
Massive Carbon Dioxide Embolism Caused by a Carbon Dioxide Blower During the Repair of a Coronary Vein During Off-Pump Coronary Artery Bypass Jong-Hwan Lee, MD, Seung-Zhoo Yoon, MD, Ju-Youn Choi, MD, Jae-Hyon Bahk, MD, and Yunseok Jeon, MD
M
AINTAINING CARDIOVASCULAR STABILITY is one of the major goals of anesthetic management of off-pump coronary artery bypass graft (OPCAB) surgery. This requires accurate diagnosis and management of the causes of cardiovascular instability. Gas embolism is a very rare cause of hypotension during OPCAB, but there have been several reports of gas embolism during endoscopic saphenectomy for coronary artery bypass grafting.1-3 In this case report, the authors describe a CO2 embolism caused by a CO2 blower while repairing an injury to a coronary vein during OPCAB. A CO2 blower was used to enhance visualization by deflecting blood away from the anastomotic site on the beating heart.4,5 This is the first case of gas embolism caused by this technique reported in the literature. CASE REPORT A 60-year-old man was admitted with a 3-month history of chest pain and progressive dyspnea on exertion. His past medical history was negative. He was taking aspirin, nitrate, captopril, and carvedilol. He was scheduled for OPCAB surgery for his unstable angina pectoris. Systolic ventricular function was normal (ejection fraction was 57%) on preoperative echocardiography. Coronary angiography revealed 95% stenosis of the distal left anterior descending artery, 99% stenosis of the proximal circumflex artery, and 99% stenosis of the right coronary artery. Anesthesia was induced with intravenous midazolam, 5 mg, etomidate, 10 mg, sufentanil, 100 g, and vecuronium, 10 mg. It was maintained with continuous infusions of sufentanil, midazolam, and vecuronium. A pulmonary artery catheter (PAC) was placed through the right internal jugular vein, and a transesophageal echocardiographic (TEE) probe was inserted. Median sternotomy was performed followed by dissection and preparation of the left internal thoracic artery. The left internal thoracic artery was then anastomosed to the left anterior descending artery without hemodynamic instability. At that time, blood gas values (pH 7.40, PO2, 180 mmHg; PCO2, 36 mmHg, and fraction of inspired oxygen, 0.5) were within normal limits, and the end-tidal CO2 was 32 mmHg. The patient was placed in the Trendelenburg position, and the heart was elevated with pericardial retraction to expose the obtuse marginal artery. During dissection of this vessel, the adjacent coronary vein was torn. The surgeon tried to suture the torn site while using a CO2 blower to maintain a clear surgical field. Although the operator observed bubbles pass through the coronary vein, the procedure was continued without informing the anesthesiologists, assuming that small amounts of CO2 in the venous system would not cause any clinical problems. About 3 minutes after application of the CO2 blower to the injured vessel, the systolic arterial pressure decreased from 100 to 50 mmHg, and the mean pulmonary arterial pressure and central venous pressure increased from 30 and 15 mmHg to 39 and 21 mmHg, respectively (Fig 1). In order to achieve hemodynamic stability, epinephrine, 30 g, vasopressin, 0.2 U, and milrinone, 2.5 mg, were administered intravenously (Fig 1A). At the same time, a sudden decrease in oxygen saturation from 100% to 50% and a decrease (Fig 2) in end-tidal CO2 from 28 mmHg to 8 mmHg (Fig 3) occurred. An arterial blood gas showed hypoxia and hypercapnia (pH 7.02, PO2, 40 mmHg, PCO2, 53 mmHg, and fraction of inspired oxygen, 1.0).
TEE examination showed that there were numerous gas bubbles in the right atrium (Fig 4), the right ventricle, and the pulmonary artery (Video 1). However, there were no gas bubbles in the left side of the heart. TEE examination also showed that there was a hyperdynamic and hypovolemic left ventricle (Video 2). The CO2 blower was immediately discontinued, and the lungs were ventilated with 100% oxygen. Aspiration from the PAC was attempted because the gas bubbles were most abundant in the pulmonary artery on the transesophageal echocardiogram. However, the amount of gas aspirated from the PAC was only 3 to 4 mL (Fig 1C). Simultaneously, epinephrine, 30 g, vasopressin, 0.2 U, and calcium chloride, 300 mg, were also administered (Fig 1B) followed by the systolic arterial pressure increasing to 98 mmHg and the pulmonary arterial pressure decreasing to 26 mmHg and central venous pressure to 10 mmHg. Although hemodynamic stability was achieved, cardiopulmonary bypass was initiated to suture the coronary vein and perform the remaining bypass procedures (Fig 1D). After the completion of all procedures, the patient was weaned uneventfully from cardiopulmonary bypass. Fluid administration consisted of 6,000 mL of crystalloid, 6 U of packed red blood cells, 3 U of fresh frozen plasma, and 10 U of platelet concentrates. The total estimated blood loss was 2,500 mL. The postoperative course was unremarkable, and the patient was discharged from the surgical intensive care unit on postoperative day 3 and from the hospital on postoperative day 7. DISCUSSION
This is the first case report that shows that the use of a CO2 blower during an OPCAB procedure can cause massive CO2 emboli with significant hemodynamic deterioration. The primary objective of surgical revascularization for ischemic heart disease is a precise and effective coronary artery anastomosis. Bleeding from the coronary arteriotomy site or coronary veins hinders precise suture placement in the often small and diffusely diseased vessels. Several techniques, such as the use of a gas blower, intraluminal coronary shunts or occluders, or intermittent irrigation with saline solution, have been used to improve visualization of the anastomotic site.6 Although the optimal method of arteriotomy visualization has not been identified, a gas blower can be effective in maintaining a bloodless field.4 Although the commonly used gases are associated with hypothetical risks including flammability, hypercarbia, and embolism,6 the authors could not find any report of a CO2 blower causing gas embolism during cardiac surgery. The main reason for the problem in the present case may have been because of the CO2 blower being used to repair a torn vein instead of an artery because the venous system has much less pressure compared with the arterial system.
From the Department of Anesthesiology, Seoul National University Hospital, Seoul, Korea. Address reprint requests to Yunseok Jeon, MD, Department of Anesthesiology, Seoul National University Hospital, 28 Yongon-Dong, Chongno-Gu, Seoul 110-744, Korea. E-mail: [email protected] © 2007 Elsevier Inc. All rights reserved. 1053-0770/07/2105-0018$32.00/0 doi:10.1053/j.jvca.2006.09.005 Key words: coronary artery bypass, off-pump, echocardiography, transesophageal
Journal of Cardiothoracic and Vascular Anesthesia, Vol 21, No 5 (October), 2007: pp 715-717
715
716
LEE ET AL
Fig 1. Changes in mean blood pressure, central venous pressure, and mean pulmonary artery pressure during CO2 embolism. (A) Epinephrine, 30 g, vasopressin, 0.2 IU, and milrinone, 2.5 mg, were administered intravenously. (B) Epinephrine, 30 g, vasopressin, 0.2 IU, and calcium chloride, 300 mg, were additionally administered. (C) Aspiration of gas was tried via pulmonary artery catheter. (D) Cardiopulmonary bypass was started.
CO2 embolism is produced from absorption of CO2 into the circulation because it is highly soluble in blood. In the presence of relative hypovolemia, CO2 may directly enter into the vascular bed with an injury to a vessel.1 In this case, direct entry of CO2 can lead to obstruction of right ventricular ejection, right- and left-sided cardiac failure, paradoxic embolism, arrhythmias, pulmonary hypertension, systemic hypotension, and cardiovascular collapse through a gas-lock effect.1 Usually, microembolism of CO2 is well tolerated because of the rapid and complete solubility of CO2, but gross embolization may overwhelm the vasculature and cause devastating results.3 With CO2 embolism, the dissolved CO2 may first increase the end-tidal CO2, and later decrease cardiac output with physiologic obstruction of pulmonary artery branch vessels by bub-
Fig 2.
Changes in end-tidal CO2 during CO2 embolism.
Fig 3.
Changes in oxygen saturation during CO2 embolism.
bles, increase physiologic deadspace, and decrease the endtidal CO2. Thus, CO2 embolism should be suspected when an increase in end-tidal CO2 is followed by a decrease in cardiac output and hypotension.1 In this case, there was no evidence of hypercapnia on the end-tidal CO2 monitor, and it is suspected that the increased physiologic deadspace was predominant compared with the effect of dissolved CO2. The transesophageal echocardiogram clearly identified a massive amount of gas in the heart. The authors tried to aspirate the gas from the distal port of the PAC. In several previous studies, the superior vena cava– right atrial junction was considered for the air aspiration using a central venous catheter.7-9 However, they were mainly studies on neurosurgical patients. The position of the patient and the route of aspiration were different from this case. Considering these reasons and the results of the TEE examination, there was no attempt to aspirate the gas at the atrial-caval junction. Hemodynamic stability was achieved primarily with pharmacologic means.
Fig 4. Transesophageal echocardiographic 2-dimensional examination from the midesophageal inflow-outflow view. There are gas bubbles in the right atrium.
MASSIVE CARBON DIOXIDE EMBOLISM
717
In conclusion, this case shows that a CO2 blower should not be applied to an injured vein for the purpose of maintaining a clear surgical field because it may cause a massive CO2 embo-
lism. It should also be noted that the transesophageal echocardiogram played a useful role in diagnosing the cause of cardiovascular instability during OPCAB.
REFERENCES 1. Martineau A, Arcand G, Couture P, et al: Transesophageal echocardiographic diagnosis of carbon dioxide embolism during minimally invasive saphenous vein harvesting and treatment with inhaled epoprostenol. Anesth Analg 96:962-964, 2003 2. Banks TA, Manetta F, Glick M, et al: Carbon dioxide embolism during minimally invasive vein harvesting. Ann Thorac Surg 73:296297, 2002 3. Kypson AP, Greenville NC: Sudden cardiac arrest after coronary artery bypass grafting as a result of massive carbon dioxide embolism. J Thorac Cardiovasc Surg 130:936-937, 2005 4. Teoh KH, Panos AL, Harmantas AA, et al: Optimal visualization of coronary artery anastomoses by gas jet. Ann Thoracic Surg 52:564, 1991 5. Sasaguri S, Hosoda Y, Yamamoto S: Carbon dioxide gas blower
for the safe visualization of coronary artery anastomosis. Ann Thorac Surg 60:1861, 1995 6. Burfeind WR Jr, Duhaylongsod FG, Annex BH, et al: High-flow gas insufflation to facilitate MIDCABG: Effects on coronary endothelium. Ann Thorac Surg 66:1246-1249, 1998 7. Domaingue CM: Anaesthesia for neurosurgery in the sitting position: A practical approach. Anaesth Intensive Care 33:323-331, 2005 8. Hanna PG, Gravenstein N, Pashayan AG: In vitro comparison of central venous catheters for aspiration of venous air embolism: Effect of catheter type, catheter tip position, and cardiac inclination. J Clin Anesth 3:290-294, 1991 9. Artru AA: Venous air embolism in prone dogs positioned with the abdomen hanging freely: Percentage of gas retrieved and success rate of resuscitation. Anesth Analg 75:715-719, 1992
M
AINTAINING CARDIOVASCULAR STABILITY is one of the major goals of anesthetic management of off-pump coronary artery bypass graft (OPCAB) surgery. This requires accurate diagnosis and management of the causes of cardiovascular instability. Gas embolism is a very rare cause of hypotension during OPCAB, but there have been several reports of gas embolism during endoscopic saphenectomy for coronary artery bypass grafting.1-3 In this case report, the authors describe a CO2 embolism caused by a CO2 blower while repairing an injury to a coronary vein during OPCAB. A CO2 blower was used to enhance visualization by deflecting blood away from the anastomotic site on the beating heart.4,5 This is the first case of gas embolism caused by this technique reported in the literature. CASE REPORT A 60-year-old man was admitted with a 3-month history of chest pain and progressive dyspnea on exertion. His past medical history was negative. He was taking aspirin, nitrate, captopril, and carvedilol. He was scheduled for OPCAB surgery for his unstable angina pectoris. Systolic ventricular function was normal (ejection fraction was 57%) on preoperative echocardiography. Coronary angiography revealed 95% stenosis of the distal left anterior descending artery, 99% stenosis of the proximal circumflex artery, and 99% stenosis of the right coronary artery. Anesthesia was induced with intravenous midazolam, 5 mg, etomidate, 10 mg, sufentanil, 100 g, and vecuronium, 10 mg. It was maintained with continuous infusions of sufentanil, midazolam, and vecuronium. A pulmonary artery catheter (PAC) was placed through the right internal jugular vein, and a transesophageal echocardiographic (TEE) probe was inserted. Median sternotomy was performed followed by dissection and preparation of the left internal thoracic artery. The left internal thoracic artery was then anastomosed to the left anterior descending artery without hemodynamic instability. At that time, blood gas values (pH 7.40, PO2, 180 mmHg; PCO2, 36 mmHg, and fraction of inspired oxygen, 0.5) were within normal limits, and the end-tidal CO2 was 32 mmHg. The patient was placed in the Trendelenburg position, and the heart was elevated with pericardial retraction to expose the obtuse marginal artery. During dissection of this vessel, the adjacent coronary vein was torn. The surgeon tried to suture the torn site while using a CO2 blower to maintain a clear surgical field. Although the operator observed bubbles pass through the coronary vein, the procedure was continued without informing the anesthesiologists, assuming that small amounts of CO2 in the venous system would not cause any clinical problems. About 3 minutes after application of the CO2 blower to the injured vessel, the systolic arterial pressure decreased from 100 to 50 mmHg, and the mean pulmonary arterial pressure and central venous pressure increased from 30 and 15 mmHg to 39 and 21 mmHg, respectively (Fig 1). In order to achieve hemodynamic stability, epinephrine, 30 g, vasopressin, 0.2 U, and milrinone, 2.5 mg, were administered intravenously (Fig 1A). At the same time, a sudden decrease in oxygen saturation from 100% to 50% and a decrease (Fig 2) in end-tidal CO2 from 28 mmHg to 8 mmHg (Fig 3) occurred. An arterial blood gas showed hypoxia and hypercapnia (pH 7.02, PO2, 40 mmHg, PCO2, 53 mmHg, and fraction of inspired oxygen, 1.0).
TEE examination showed that there were numerous gas bubbles in the right atrium (Fig 4), the right ventricle, and the pulmonary artery (Video 1). However, there were no gas bubbles in the left side of the heart. TEE examination also showed that there was a hyperdynamic and hypovolemic left ventricle (Video 2). The CO2 blower was immediately discontinued, and the lungs were ventilated with 100% oxygen. Aspiration from the PAC was attempted because the gas bubbles were most abundant in the pulmonary artery on the transesophageal echocardiogram. However, the amount of gas aspirated from the PAC was only 3 to 4 mL (Fig 1C). Simultaneously, epinephrine, 30 g, vasopressin, 0.2 U, and calcium chloride, 300 mg, were also administered (Fig 1B) followed by the systolic arterial pressure increasing to 98 mmHg and the pulmonary arterial pressure decreasing to 26 mmHg and central venous pressure to 10 mmHg. Although hemodynamic stability was achieved, cardiopulmonary bypass was initiated to suture the coronary vein and perform the remaining bypass procedures (Fig 1D). After the completion of all procedures, the patient was weaned uneventfully from cardiopulmonary bypass. Fluid administration consisted of 6,000 mL of crystalloid, 6 U of packed red blood cells, 3 U of fresh frozen plasma, and 10 U of platelet concentrates. The total estimated blood loss was 2,500 mL. The postoperative course was unremarkable, and the patient was discharged from the surgical intensive care unit on postoperative day 3 and from the hospital on postoperative day 7. DISCUSSION
This is the first case report that shows that the use of a CO2 blower during an OPCAB procedure can cause massive CO2 emboli with significant hemodynamic deterioration. The primary objective of surgical revascularization for ischemic heart disease is a precise and effective coronary artery anastomosis. Bleeding from the coronary arteriotomy site or coronary veins hinders precise suture placement in the often small and diffusely diseased vessels. Several techniques, such as the use of a gas blower, intraluminal coronary shunts or occluders, or intermittent irrigation with saline solution, have been used to improve visualization of the anastomotic site.6 Although the optimal method of arteriotomy visualization has not been identified, a gas blower can be effective in maintaining a bloodless field.4 Although the commonly used gases are associated with hypothetical risks including flammability, hypercarbia, and embolism,6 the authors could not find any report of a CO2 blower causing gas embolism during cardiac surgery. The main reason for the problem in the present case may have been because of the CO2 blower being used to repair a torn vein instead of an artery because the venous system has much less pressure compared with the arterial system.
From the Department of Anesthesiology, Seoul National University Hospital, Seoul, Korea. Address reprint requests to Yunseok Jeon, MD, Department of Anesthesiology, Seoul National University Hospital, 28 Yongon-Dong, Chongno-Gu, Seoul 110-744, Korea. E-mail: [email protected] © 2007 Elsevier Inc. All rights reserved. 1053-0770/07/2105-0018$32.00/0 doi:10.1053/j.jvca.2006.09.005 Key words: coronary artery bypass, off-pump, echocardiography, transesophageal
Journal of Cardiothoracic and Vascular Anesthesia, Vol 21, No 5 (October), 2007: pp 715-717
715
716
LEE ET AL
Fig 1. Changes in mean blood pressure, central venous pressure, and mean pulmonary artery pressure during CO2 embolism. (A) Epinephrine, 30 g, vasopressin, 0.2 IU, and milrinone, 2.5 mg, were administered intravenously. (B) Epinephrine, 30 g, vasopressin, 0.2 IU, and calcium chloride, 300 mg, were additionally administered. (C) Aspiration of gas was tried via pulmonary artery catheter. (D) Cardiopulmonary bypass was started.
CO2 embolism is produced from absorption of CO2 into the circulation because it is highly soluble in blood. In the presence of relative hypovolemia, CO2 may directly enter into the vascular bed with an injury to a vessel.1 In this case, direct entry of CO2 can lead to obstruction of right ventricular ejection, right- and left-sided cardiac failure, paradoxic embolism, arrhythmias, pulmonary hypertension, systemic hypotension, and cardiovascular collapse through a gas-lock effect.1 Usually, microembolism of CO2 is well tolerated because of the rapid and complete solubility of CO2, but gross embolization may overwhelm the vasculature and cause devastating results.3 With CO2 embolism, the dissolved CO2 may first increase the end-tidal CO2, and later decrease cardiac output with physiologic obstruction of pulmonary artery branch vessels by bub-
Fig 2.
Changes in end-tidal CO2 during CO2 embolism.
Fig 3.
Changes in oxygen saturation during CO2 embolism.
bles, increase physiologic deadspace, and decrease the endtidal CO2. Thus, CO2 embolism should be suspected when an increase in end-tidal CO2 is followed by a decrease in cardiac output and hypotension.1 In this case, there was no evidence of hypercapnia on the end-tidal CO2 monitor, and it is suspected that the increased physiologic deadspace was predominant compared with the effect of dissolved CO2. The transesophageal echocardiogram clearly identified a massive amount of gas in the heart. The authors tried to aspirate the gas from the distal port of the PAC. In several previous studies, the superior vena cava– right atrial junction was considered for the air aspiration using a central venous catheter.7-9 However, they were mainly studies on neurosurgical patients. The position of the patient and the route of aspiration were different from this case. Considering these reasons and the results of the TEE examination, there was no attempt to aspirate the gas at the atrial-caval junction. Hemodynamic stability was achieved primarily with pharmacologic means.
Fig 4. Transesophageal echocardiographic 2-dimensional examination from the midesophageal inflow-outflow view. There are gas bubbles in the right atrium.
MASSIVE CARBON DIOXIDE EMBOLISM
717
In conclusion, this case shows that a CO2 blower should not be applied to an injured vein for the purpose of maintaining a clear surgical field because it may cause a massive CO2 embo-
lism. It should also be noted that the transesophageal echocardiogram played a useful role in diagnosing the cause of cardiovascular instability during OPCAB.
REFERENCES 1. Martineau A, Arcand G, Couture P, et al: Transesophageal echocardiographic diagnosis of carbon dioxide embolism during minimally invasive saphenous vein harvesting and treatment with inhaled epoprostenol. Anesth Analg 96:962-964, 2003 2. Banks TA, Manetta F, Glick M, et al: Carbon dioxide embolism during minimally invasive vein harvesting. Ann Thorac Surg 73:296297, 2002 3. Kypson AP, Greenville NC: Sudden cardiac arrest after coronary artery bypass grafting as a result of massive carbon dioxide embolism. J Thorac Cardiovasc Surg 130:936-937, 2005 4. Teoh KH, Panos AL, Harmantas AA, et al: Optimal visualization of coronary artery anastomoses by gas jet. Ann Thoracic Surg 52:564, 1991 5. Sasaguri S, Hosoda Y, Yamamoto S: Carbon dioxide gas blower
for the safe visualization of coronary artery anastomosis. Ann Thorac Surg 60:1861, 1995 6. Burfeind WR Jr, Duhaylongsod FG, Annex BH, et al: High-flow gas insufflation to facilitate MIDCABG: Effects on coronary endothelium. Ann Thorac Surg 66:1246-1249, 1998 7. Domaingue CM: Anaesthesia for neurosurgery in the sitting position: A practical approach. Anaesth Intensive Care 33:323-331, 2005 8. Hanna PG, Gravenstein N, Pashayan AG: In vitro comparison of central venous catheters for aspiration of venous air embolism: Effect of catheter type, catheter tip position, and cardiac inclination. J Clin Anesth 3:290-294, 1991 9. Artru AA: Venous air embolism in prone dogs positioned with the abdomen hanging freely: Percentage of gas retrieved and success rate of resuscitation. Anesth Analg 75:715-719, 1992