e6
LETTERS TO THE EDITOR
LA RA
LA Ao
Ao LV
Fig 3. Successful closure of ruptured noncoronary sinus of Valsalva aneurysm. 2D imaging reveals A. lack of residual shunt, and B. no new aortic valve dysfunction. Abbreviations: Ao, aorta; LA, left atrium; LV, left ventricle; RA, right atrium. Arrow indicates device.
multiple planes, allowing for more accurate anatomic detail and revealing that the aneurysm was in the non-coronary sinus, not the right coronary sinus as the preoperative 2D TTE erroneously had diagnosed. While improvement in outcomes with 3D TEE over 2D TEE will be difficult to prove, live 3D TEE imaging does indeed allow for precise visualization of complex spatial relationships between critical anatomic structures, which may be out-of-plane when using 2D imaging modalities. Indeed, while passing the guidewire across the ruptured sinus of Valsalva, the only imaging modality that definitively showed the wire in both the aorta and the right atrium was 3D TEE (Fig 1, BCD). 3D TEE thus allowed safe, effective, and efficient navigation of the device to the site of the defect while reducing use of fluoroscopy and exposure to ionizing radiation. As percutaneous techniques in the cardiac catheterization laboratory become more common, there likely will be an increasing role for 3D TEE in both diagnosis and operative management of these lesions.
Jason H. Chua, MD Emily Methangkool, MD Catherine M. Cha, MD Aman Mahajan, MD, PhD Department of Anesthesiology, David Geffen School of Medicine at UCLA, University of California Los Angeles (UCLA), Los Angeles, CA
REFERENCES 1. Mukherjee C, Hein F, Holzhey D, et al: Is real time 3D transesophageal echocardiography a feasible approach to detect coronary ostium during transapical aortic valve implantation. J Cardiothorac Vasc Anesth 27:654-659, 2013 2. Arora R, Trehan V, Rangasetty UM, et al: Transcatheter closure of ruptured sinus of Valsalva aneurysm. J Interven Cardiol 17:53-58, 2004 3. Zhao SH, Yan CW, Zhu XY, et al: Transcatheter occlusion of the ruptured sinus of Valsalva aneurysm with an Amplatzer duct occluder. Int J Cardiol 129:81-85, 2008 4. Fishbein MC, Obma R, Roberts WC: Unruptured sinus of Valsalva aneurysm. Am J Cardiol 35:918-922, 1975 5. Feldman DN, Roman MJ: Aneurysms of the sinuses of Valsalva. Cardiology 106:73-81, 2006 6. Chu SH, Hung CR, How SS, et al: Ruptured aneurysms of the sinus of Valsalva in oriental patients. J Thorac Cardiovasc Surg 99:288-298, 1990
7. Munk M, Gatzoulis MA, King DE, et al: Cardiac tamponade and death from intrapericardial rupture of sinus of Valsalva aneurysm. Eur J Cardiothorac Surg 15:100-102, 1999 8. Arora R, Trehan V, Rangasetty UM, et al: Transcatheter closure of ruptured sinus of Valsalva aneurysm. J Interven Cardiol 17:53-58, 2004 9. Zhao SH, Yan CW, Zhu XY, et al: Transcatheter occlusion of the ruptured sinus of Valsalva aneurysm with an Amplatzer duct occluder. Int J Cardiol 129:81-85, 2008 10. Takach TJ, Reul GJ, Duncan JM, et al: Sinus of Valsalva aneurysm or fistula: Management and outcome. Ann Thorac Surg 68: 1573-1577, 1999 11. Cullen S, Somerville J, Redington A: Transcatheter closure of ruptured aneurysm of sinus of Valsalva. Br Heart J 71:479-480, 1994 12. Raslan S, Nanda NC, Lloyd L: Incremental value of live/real time three-dimensional transesophageal echocardiography over the two-dimensional technique in the assessment of sinus of Valsalva aneurysm rupture. Echo 28:918-920, 2011 13. Oh-Icí D, Malergue M, Garot J, et al: Sinus of Valsalva rupture: Percutaneous closure with real-time 3-dimensional echocardiography. J Am Coll Cardiol 56:e31, 2010 14. Chandra S, Vijay SK, Dwivedi SK, et al: Delineation of anatomy of the ruptured sinus of Valsalva with three-dimensional echocardiography: The advantage of the added dimension. Echo 29:E148-E151, 2012 15. Jean WH, Kang TJ, Liu CM, et al: Transcatheter occlusion of ruptured sinus of Valsalva aneurysm guided by three-dimensional transesophageal echocardiography. J Formos Med Assoc 103:948-951, 2004 http://dx.doi.org/10.1053/j.jvca.2013.08.022
Safety and Utility of Noninvasive Ventilation During Deep Sedation for Catheter Ablation of Atrial Fibrillation To the Editor: We read with interest the article by Elkassabany et al, entitled “Anesthetic management of patients undergoing pulmonary vein isolation for treatment of atrial fibrillation using high-frequency jet ventilation.”1 We wish to share our experience in the context of using noninvasive ventilation (NIV) during deep sedation to render the procedure safer and more comfortable for patients undergoing a long procedure that requires motionlessness. This
e7
LETTERS TO THE EDITOR
Fig 1. (A) Garbin ventilator. (B) Respironic latex-free total face mask.
retrospective study was conducted in a single high-volume electrophysiology procedure center, and 41 consecutive catheter ablation for paroxysmal/persistent atrial fibrillation2 procedures performed with deep sedation using NIV were evaluated. Sedation procedures were performed according to SIAARTI3 guidelines. During the procedure, routine monitoring, including invasive arterial pressure and serial arterial blood gas analyses, was performed. Midazolam (0.01-0.02 mg/kg IV) was administered immediately before monitoring, and fentanyl (5-7 mg/kg) was administered as an analgesic. Sedation (propofol infusion: bolus dose 1-2 mg/kg, maintenance 2-5 mg/kg/h) and NIV were performed after trans-septal puncture to rule out left-sided emboli through neurologic assessment. NIV ventilation (Fig 1) was performed with a Respironic latex-free total face mask (Murrysville, Pennsylvania) connected to a Garbin ventilator (Linde Inc., Herrsching, Germany) in spontaneous/temporized mode, applying incorporated algorithms to improve patient-ventilator synchrony by adjusting to changing breathing patterns and dynamic leaks. I-PAP, E-PAP, and respiratory rate were modified according to the clinical response, including tolerance of the patient to obtain an exhaled tidal volume of 6 to 8 mL/kg; FIO2 requirement was 40% or less to maintain the oxygen saturation above 92%. Sedation and mechanical ventilation were discontinued at the end of the catheter ablation procedure. The clinical characteristics of the patients and the procedural detail are shown in Table I. During the procedures, no respiratory complications were observed. Furthermore, there were no problems due to mask-related difficulties, gastric distention, NIV discomfort, or significant hemodynamic alterations related to positive-pressure ventilation. Adverse events were reported in 13 patients (32%). Only exacerbation of bronchial asthma (2/13) was related to anesthetic management; these patients responded rapidly to treatment with inhaled β2-agonists and showed no alterations in chest x-rays compatible with bronchopneumonia. The other problems were due to the electrophysiologic procedure, and although they have occurred with an incidence greater than expected, major complications (2/13) were comparable.4 The safety of deep sedation during atrial fibrillation ablation has been described,5 but in this case series, a lower impact of NIV on arterial blood gas tensions and pH balance6 was observed. Using NIV in this context, as in others,7,8 it is possible
Table I. Clinical characteristics of patients Characteristic
Age (years) Male gender, n (%) Hypertension, n (%) Diabetes, n (%) Smoke exposure, n (%) Current smoke exposure, n (%) ASA I, n (%) ASA II, n (%) NYHA functional class I, n (%) NYHA functional class II, n (%) Weight (Kg) Height (cm) Body Mass Index Left ventricular ejection fraction, n (%) Length of catheter ablation procedure, min Time of anesthesia/NIV, min Basal pH Basal PaO2 (mmHg) Basal PaCO2 (mmHg) Basal HCO-3 (mmol/L) Intraprocedural pH Intraprocedural PaO2 (mmHg) Intraprocedural PaCO2 (mmHg) Intraprocedural HCO-3 (mmol/L) Δ pH (basal to intraprocedural,% change) Δ PaO2 (basal to intraprocedural,% change) Δ PaCO2 (basal to intraprocedural,% change) Δ HCO-3 (basal to intraprocedural,% change) Procedural complication, n (%) Pleuro-pericardial effusion, n Vascular access complication*, n Exacerbation of bronchial asthma, n Bradyarrhythmia requiring definitive pacemaker implantation, n Pulmonary embolism, n Recurrence of AF occurring within 48 h, n (%)
(n ¼ 41)
62 ⫾ 10 33 (81) 20 (49) 5 (12) 18 (44) 7 (17) 2 (5) 39 (95) 23 (56) 18 (44) 81 ⫾ 16 150 ⫾ 59 27 ⫾ 4 56 ⫾ 9 261 ⫾ 42 164 ⫾ 47 7.41 ⫾ 0.01 82.89 ⫾ 11.81 40.50 ⫾ 0.85 25.65 ⫾ 0.31 7.37 ⫾ 0.05 117.10 ⫾ 27.25 43.37 ⫾ 6.91 24.71 ⫾ 2.12 0.52 ⫾ 0.83 37.14 ⫾ 30.95 7.21 ⫾ 15.55 3.08 ⫾ 9.76 13 (32%) 5 4 2 1 1 11/41 (27%)
Abbreviations: AF, atrial fibrillation; ASA, American Society of Anesthesiologists physical status classification system; NIV, noninvasive ventilation; NYHA, New York Heart Association. *Iatrogenic femoral pseudoaneurysms in 2 cases and femoral hematoma with decrease in hemoglobin levels greater than 2 g/dL in 2 cases – none of these cases required transfusion support.
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to reduce the flow of oxygen administered to the patient and maintain better respiratory dynamics. These conditions allowed us to maintain effective CO2 elimination with minimum impact on the pH, reducing the risk of hemodynamic, respiratory, or neurologic problems resulting from improper ventilation without patient discomfort or risk. Furthermore, during the procedure, patient safety was ensured by the ventilator, which allowed a continuous control of tidal volume, amount of ventilation lost to leak, and effective minute ventilation. Francesco Sbrana, MD* Andrea Ripoli, PhD* Bruno Formichi, MD† *Fondazione Toscana Gabriele Monasterio, Pisa, Italy †Fondazione Toscana Gabriele Monasterio and National Research Council, Institute of Clinical Physiology, Pisa, Italy REFERENCES 1. Elkassabany N, Garcia F, Tschabrunn C, et al: Anesthetic management of patients undergoing pulmonary vein isolation for treatment of atrial fibrillation using high-frequency jet ventilation. J Cardiothorac Vasc Anesth 26:433-438, 2012 2. Calkins H, Kuck KH, Cappato R, et al: 2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for patient selection, procedural techniques, patient management and follow-up, definij;tions, endpoints, and research trial design. Europace 14:528-606, 2012 3. SIAARTI Study Group for Safety in Anesthesia and Intensive Care. Recommendations for anesthesia and sedation in nonoperating room locations. Minerva Anestesiol 71:11-20, 2005 4. Spragg DD, Dalal D, Cheema A, et al: Complications of catheter ablation for atrial fibrillation: Incidence and predictors. J Cardiovasc Electrophysiol 19:627-631, 2008 5. Kottkamp H, Hindricks G, Eitel C, et al: Deep sedation for catheter ablation of atrial fibrillation: A prospective study in 650 consecutive patients. J Cardiovasc Electrophysiol 22:1339-1343, 2011 6. Flenley DC: Arterial blood gas tensions and pH. Br J Clin Pharmacol 9:129-135, 1980 7. Guarracino F, Ambrosino N: Non invasive ventilation in cardiosurgical patients. Minerva Anestesiol 77:734-741, 2011 8. Landoni G, Zangrillo A, Cabrini L: Noninvasive ventilation after cardiac and thoracic surgery in adult patients: A review. J Cardiothorac Vasc Anesth 26:917-922, 2012 http://dx.doi.org/10.1053/j.jvca.2013.09.003
Apnea Testing for Diagnosing Brain Death During Extracorporeal Membrane Oxygenation To the Editor: Use of extracorporeal membrane oxygenation (ECMO) during cardiopulmonary resuscitation (CPR) can increase survival rates for adults and children; however, the reported risks of neurologic injury and brain death remain high (33% and 21%, respectively).1–3 Prompt diagnosis of brain death during ECMO is
essential to optimize resource usage and identify potential organ donors swiftly. The clinical criteria for brain death are irreversible coma of known cause, absent brainstem reflexes, and positive apnea test.4 However, ECMO removes carbon dioxide (CO2) efficiently; thus, it is challenging to increase partial arterial CO2 (PaCO2) and conduct an apnea test during ECMO. We describe the use of an exogenous CO2 source to increase PaCO2 during ECMO and ensure a reliable apnea test. A 65-year-old woman with a history of stage 2 breast cancer collapsed suddenly at home 2 days after surgical stripping of varicose veins in her legs. After 25 minutes of CPR, spontaneous circulation was restored, and she was transferred to intensive care. Computed tomographic pulmonary angiography revealed pulmonary embolism, and bedside echocardiography suggested massive pulmonary embolism. Despite administration of tissue plasminogen activator and vasopressors, the patient became hemodynamically unstable. She was transferred to the operating room for pulmonary thrombectomy under cardiopulmonary bypass (CPB). Thrombi were removed from the patient’s pulmonary arteries, but it was not possible to wean her from CPB. Veno-arterial (right atrium-to-femoral artery) cannulation was performed to provide ECMO. With an ECMO flow of 4 L/min, hemodynamic and metabolic stability were restored, and therapeutic hypothermia (331C) was achieved. Twenty-four hours after ECMO initiation, therapeutic hypothermia was terminated. At 55 hours and in the absence of sedation, neuromuscular-blocking agents, and hypothermia, the patient’s Glasgow coma scale score was 3, and she had no brainstem reflexes. Twenty-four hours later, her neurologic findings were unchanged and an apnea test was scheduled. To perform the apnea test, a CPB gas blender connected to a CO2 tube was incorporated into the ECMO circuit. The mechanical ventilator was set at a respiratory rate of 4 breaths/minute and FIO2 1.0. After baseline, arterial blood gases were recorded, and CO2 was added to the blender starting at 0.5 L/minute and titrating to an end-tidal CO2 of 60 mmHg. Once this target was reached, arterial blood gas analysis was repeated to confirm PaCO2. We closely observed the patient’s chest movements, the end-tidal CO2 tracing, and the ventilator for any spontaneous breathing effort. As none was detected, the apnea test was positive. Monitoring had revealed no hemodynamic changes or hypoxemia during the apnea test. Brain death was declared, and ECMO support was withdrawn. Very little has been published regarding apnea testing and diagnosis of brain death during ECMO.5,6 We believe that addition of exogenous CO2 to the gas blender is a valid method for conducting apnea tests during ECMO. Maintaining ventilatory support at a low respiratory rate and monitoring end-tidal CO2 helps in titrating the flow rate of exogenous CO2 appropriately and also improves the safety of this method.
Arash Pirat, MD Özgür Kömürcü, MD Güray Yener Gülnaz Arslan, MD Faculty of Medicine, Departments of Anesthesiology and Cardiovascular Perfusion Baskent University, Ankara, Turkey
LETTERS TO THE EDITOR
LA RA
LA Ao
Ao LV
Fig 3. Successful closure of ruptured noncoronary sinus of Valsalva aneurysm. 2D imaging reveals A. lack of residual shunt, and B. no new aortic valve dysfunction. Abbreviations: Ao, aorta; LA, left atrium; LV, left ventricle; RA, right atrium. Arrow indicates device.
multiple planes, allowing for more accurate anatomic detail and revealing that the aneurysm was in the non-coronary sinus, not the right coronary sinus as the preoperative 2D TTE erroneously had diagnosed. While improvement in outcomes with 3D TEE over 2D TEE will be difficult to prove, live 3D TEE imaging does indeed allow for precise visualization of complex spatial relationships between critical anatomic structures, which may be out-of-plane when using 2D imaging modalities. Indeed, while passing the guidewire across the ruptured sinus of Valsalva, the only imaging modality that definitively showed the wire in both the aorta and the right atrium was 3D TEE (Fig 1, BCD). 3D TEE thus allowed safe, effective, and efficient navigation of the device to the site of the defect while reducing use of fluoroscopy and exposure to ionizing radiation. As percutaneous techniques in the cardiac catheterization laboratory become more common, there likely will be an increasing role for 3D TEE in both diagnosis and operative management of these lesions.
Jason H. Chua, MD Emily Methangkool, MD Catherine M. Cha, MD Aman Mahajan, MD, PhD Department of Anesthesiology, David Geffen School of Medicine at UCLA, University of California Los Angeles (UCLA), Los Angeles, CA
REFERENCES 1. Mukherjee C, Hein F, Holzhey D, et al: Is real time 3D transesophageal echocardiography a feasible approach to detect coronary ostium during transapical aortic valve implantation. J Cardiothorac Vasc Anesth 27:654-659, 2013 2. Arora R, Trehan V, Rangasetty UM, et al: Transcatheter closure of ruptured sinus of Valsalva aneurysm. J Interven Cardiol 17:53-58, 2004 3. Zhao SH, Yan CW, Zhu XY, et al: Transcatheter occlusion of the ruptured sinus of Valsalva aneurysm with an Amplatzer duct occluder. Int J Cardiol 129:81-85, 2008 4. Fishbein MC, Obma R, Roberts WC: Unruptured sinus of Valsalva aneurysm. Am J Cardiol 35:918-922, 1975 5. Feldman DN, Roman MJ: Aneurysms of the sinuses of Valsalva. Cardiology 106:73-81, 2006 6. Chu SH, Hung CR, How SS, et al: Ruptured aneurysms of the sinus of Valsalva in oriental patients. J Thorac Cardiovasc Surg 99:288-298, 1990
7. Munk M, Gatzoulis MA, King DE, et al: Cardiac tamponade and death from intrapericardial rupture of sinus of Valsalva aneurysm. Eur J Cardiothorac Surg 15:100-102, 1999 8. Arora R, Trehan V, Rangasetty UM, et al: Transcatheter closure of ruptured sinus of Valsalva aneurysm. J Interven Cardiol 17:53-58, 2004 9. Zhao SH, Yan CW, Zhu XY, et al: Transcatheter occlusion of the ruptured sinus of Valsalva aneurysm with an Amplatzer duct occluder. Int J Cardiol 129:81-85, 2008 10. Takach TJ, Reul GJ, Duncan JM, et al: Sinus of Valsalva aneurysm or fistula: Management and outcome. Ann Thorac Surg 68: 1573-1577, 1999 11. Cullen S, Somerville J, Redington A: Transcatheter closure of ruptured aneurysm of sinus of Valsalva. Br Heart J 71:479-480, 1994 12. Raslan S, Nanda NC, Lloyd L: Incremental value of live/real time three-dimensional transesophageal echocardiography over the two-dimensional technique in the assessment of sinus of Valsalva aneurysm rupture. Echo 28:918-920, 2011 13. Oh-Icí D, Malergue M, Garot J, et al: Sinus of Valsalva rupture: Percutaneous closure with real-time 3-dimensional echocardiography. J Am Coll Cardiol 56:e31, 2010 14. Chandra S, Vijay SK, Dwivedi SK, et al: Delineation of anatomy of the ruptured sinus of Valsalva with three-dimensional echocardiography: The advantage of the added dimension. Echo 29:E148-E151, 2012 15. Jean WH, Kang TJ, Liu CM, et al: Transcatheter occlusion of ruptured sinus of Valsalva aneurysm guided by three-dimensional transesophageal echocardiography. J Formos Med Assoc 103:948-951, 2004 http://dx.doi.org/10.1053/j.jvca.2013.08.022
Safety and Utility of Noninvasive Ventilation During Deep Sedation for Catheter Ablation of Atrial Fibrillation To the Editor: We read with interest the article by Elkassabany et al, entitled “Anesthetic management of patients undergoing pulmonary vein isolation for treatment of atrial fibrillation using high-frequency jet ventilation.”1 We wish to share our experience in the context of using noninvasive ventilation (NIV) during deep sedation to render the procedure safer and more comfortable for patients undergoing a long procedure that requires motionlessness. This
e7
LETTERS TO THE EDITOR
Fig 1. (A) Garbin ventilator. (B) Respironic latex-free total face mask.
retrospective study was conducted in a single high-volume electrophysiology procedure center, and 41 consecutive catheter ablation for paroxysmal/persistent atrial fibrillation2 procedures performed with deep sedation using NIV were evaluated. Sedation procedures were performed according to SIAARTI3 guidelines. During the procedure, routine monitoring, including invasive arterial pressure and serial arterial blood gas analyses, was performed. Midazolam (0.01-0.02 mg/kg IV) was administered immediately before monitoring, and fentanyl (5-7 mg/kg) was administered as an analgesic. Sedation (propofol infusion: bolus dose 1-2 mg/kg, maintenance 2-5 mg/kg/h) and NIV were performed after trans-septal puncture to rule out left-sided emboli through neurologic assessment. NIV ventilation (Fig 1) was performed with a Respironic latex-free total face mask (Murrysville, Pennsylvania) connected to a Garbin ventilator (Linde Inc., Herrsching, Germany) in spontaneous/temporized mode, applying incorporated algorithms to improve patient-ventilator synchrony by adjusting to changing breathing patterns and dynamic leaks. I-PAP, E-PAP, and respiratory rate were modified according to the clinical response, including tolerance of the patient to obtain an exhaled tidal volume of 6 to 8 mL/kg; FIO2 requirement was 40% or less to maintain the oxygen saturation above 92%. Sedation and mechanical ventilation were discontinued at the end of the catheter ablation procedure. The clinical characteristics of the patients and the procedural detail are shown in Table I. During the procedures, no respiratory complications were observed. Furthermore, there were no problems due to mask-related difficulties, gastric distention, NIV discomfort, or significant hemodynamic alterations related to positive-pressure ventilation. Adverse events were reported in 13 patients (32%). Only exacerbation of bronchial asthma (2/13) was related to anesthetic management; these patients responded rapidly to treatment with inhaled β2-agonists and showed no alterations in chest x-rays compatible with bronchopneumonia. The other problems were due to the electrophysiologic procedure, and although they have occurred with an incidence greater than expected, major complications (2/13) were comparable.4 The safety of deep sedation during atrial fibrillation ablation has been described,5 but in this case series, a lower impact of NIV on arterial blood gas tensions and pH balance6 was observed. Using NIV in this context, as in others,7,8 it is possible
Table I. Clinical characteristics of patients Characteristic
Age (years) Male gender, n (%) Hypertension, n (%) Diabetes, n (%) Smoke exposure, n (%) Current smoke exposure, n (%) ASA I, n (%) ASA II, n (%) NYHA functional class I, n (%) NYHA functional class II, n (%) Weight (Kg) Height (cm) Body Mass Index Left ventricular ejection fraction, n (%) Length of catheter ablation procedure, min Time of anesthesia/NIV, min Basal pH Basal PaO2 (mmHg) Basal PaCO2 (mmHg) Basal HCO-3 (mmol/L) Intraprocedural pH Intraprocedural PaO2 (mmHg) Intraprocedural PaCO2 (mmHg) Intraprocedural HCO-3 (mmol/L) Δ pH (basal to intraprocedural,% change) Δ PaO2 (basal to intraprocedural,% change) Δ PaCO2 (basal to intraprocedural,% change) Δ HCO-3 (basal to intraprocedural,% change) Procedural complication, n (%) Pleuro-pericardial effusion, n Vascular access complication*, n Exacerbation of bronchial asthma, n Bradyarrhythmia requiring definitive pacemaker implantation, n Pulmonary embolism, n Recurrence of AF occurring within 48 h, n (%)
(n ¼ 41)
62 ⫾ 10 33 (81) 20 (49) 5 (12) 18 (44) 7 (17) 2 (5) 39 (95) 23 (56) 18 (44) 81 ⫾ 16 150 ⫾ 59 27 ⫾ 4 56 ⫾ 9 261 ⫾ 42 164 ⫾ 47 7.41 ⫾ 0.01 82.89 ⫾ 11.81 40.50 ⫾ 0.85 25.65 ⫾ 0.31 7.37 ⫾ 0.05 117.10 ⫾ 27.25 43.37 ⫾ 6.91 24.71 ⫾ 2.12 0.52 ⫾ 0.83 37.14 ⫾ 30.95 7.21 ⫾ 15.55 3.08 ⫾ 9.76 13 (32%) 5 4 2 1 1 11/41 (27%)
Abbreviations: AF, atrial fibrillation; ASA, American Society of Anesthesiologists physical status classification system; NIV, noninvasive ventilation; NYHA, New York Heart Association. *Iatrogenic femoral pseudoaneurysms in 2 cases and femoral hematoma with decrease in hemoglobin levels greater than 2 g/dL in 2 cases – none of these cases required transfusion support.
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to reduce the flow of oxygen administered to the patient and maintain better respiratory dynamics. These conditions allowed us to maintain effective CO2 elimination with minimum impact on the pH, reducing the risk of hemodynamic, respiratory, or neurologic problems resulting from improper ventilation without patient discomfort or risk. Furthermore, during the procedure, patient safety was ensured by the ventilator, which allowed a continuous control of tidal volume, amount of ventilation lost to leak, and effective minute ventilation. Francesco Sbrana, MD* Andrea Ripoli, PhD* Bruno Formichi, MD† *Fondazione Toscana Gabriele Monasterio, Pisa, Italy †Fondazione Toscana Gabriele Monasterio and National Research Council, Institute of Clinical Physiology, Pisa, Italy REFERENCES 1. Elkassabany N, Garcia F, Tschabrunn C, et al: Anesthetic management of patients undergoing pulmonary vein isolation for treatment of atrial fibrillation using high-frequency jet ventilation. J Cardiothorac Vasc Anesth 26:433-438, 2012 2. Calkins H, Kuck KH, Cappato R, et al: 2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for patient selection, procedural techniques, patient management and follow-up, definij;tions, endpoints, and research trial design. Europace 14:528-606, 2012 3. SIAARTI Study Group for Safety in Anesthesia and Intensive Care. Recommendations for anesthesia and sedation in nonoperating room locations. Minerva Anestesiol 71:11-20, 2005 4. Spragg DD, Dalal D, Cheema A, et al: Complications of catheter ablation for atrial fibrillation: Incidence and predictors. J Cardiovasc Electrophysiol 19:627-631, 2008 5. Kottkamp H, Hindricks G, Eitel C, et al: Deep sedation for catheter ablation of atrial fibrillation: A prospective study in 650 consecutive patients. J Cardiovasc Electrophysiol 22:1339-1343, 2011 6. Flenley DC: Arterial blood gas tensions and pH. Br J Clin Pharmacol 9:129-135, 1980 7. Guarracino F, Ambrosino N: Non invasive ventilation in cardiosurgical patients. Minerva Anestesiol 77:734-741, 2011 8. Landoni G, Zangrillo A, Cabrini L: Noninvasive ventilation after cardiac and thoracic surgery in adult patients: A review. J Cardiothorac Vasc Anesth 26:917-922, 2012 http://dx.doi.org/10.1053/j.jvca.2013.09.003
Apnea Testing for Diagnosing Brain Death During Extracorporeal Membrane Oxygenation To the Editor: Use of extracorporeal membrane oxygenation (ECMO) during cardiopulmonary resuscitation (CPR) can increase survival rates for adults and children; however, the reported risks of neurologic injury and brain death remain high (33% and 21%, respectively).1–3 Prompt diagnosis of brain death during ECMO is
essential to optimize resource usage and identify potential organ donors swiftly. The clinical criteria for brain death are irreversible coma of known cause, absent brainstem reflexes, and positive apnea test.4 However, ECMO removes carbon dioxide (CO2) efficiently; thus, it is challenging to increase partial arterial CO2 (PaCO2) and conduct an apnea test during ECMO. We describe the use of an exogenous CO2 source to increase PaCO2 during ECMO and ensure a reliable apnea test. A 65-year-old woman with a history of stage 2 breast cancer collapsed suddenly at home 2 days after surgical stripping of varicose veins in her legs. After 25 minutes of CPR, spontaneous circulation was restored, and she was transferred to intensive care. Computed tomographic pulmonary angiography revealed pulmonary embolism, and bedside echocardiography suggested massive pulmonary embolism. Despite administration of tissue plasminogen activator and vasopressors, the patient became hemodynamically unstable. She was transferred to the operating room for pulmonary thrombectomy under cardiopulmonary bypass (CPB). Thrombi were removed from the patient’s pulmonary arteries, but it was not possible to wean her from CPB. Veno-arterial (right atrium-to-femoral artery) cannulation was performed to provide ECMO. With an ECMO flow of 4 L/min, hemodynamic and metabolic stability were restored, and therapeutic hypothermia (331C) was achieved. Twenty-four hours after ECMO initiation, therapeutic hypothermia was terminated. At 55 hours and in the absence of sedation, neuromuscular-blocking agents, and hypothermia, the patient’s Glasgow coma scale score was 3, and she had no brainstem reflexes. Twenty-four hours later, her neurologic findings were unchanged and an apnea test was scheduled. To perform the apnea test, a CPB gas blender connected to a CO2 tube was incorporated into the ECMO circuit. The mechanical ventilator was set at a respiratory rate of 4 breaths/minute and FIO2 1.0. After baseline, arterial blood gases were recorded, and CO2 was added to the blender starting at 0.5 L/minute and titrating to an end-tidal CO2 of 60 mmHg. Once this target was reached, arterial blood gas analysis was repeated to confirm PaCO2. We closely observed the patient’s chest movements, the end-tidal CO2 tracing, and the ventilator for any spontaneous breathing effort. As none was detected, the apnea test was positive. Monitoring had revealed no hemodynamic changes or hypoxemia during the apnea test. Brain death was declared, and ECMO support was withdrawn. Very little has been published regarding apnea testing and diagnosis of brain death during ECMO.5,6 We believe that addition of exogenous CO2 to the gas blender is a valid method for conducting apnea tests during ECMO. Maintaining ventilatory support at a low respiratory rate and monitoring end-tidal CO2 helps in titrating the flow rate of exogenous CO2 appropriately and also improves the safety of this method.
Arash Pirat, MD Özgür Kömürcü, MD Güray Yener Gülnaz Arslan, MD Faculty of Medicine, Departments of Anesthesiology and Cardiovascular Perfusion Baskent University, Ankara, Turkey
